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<h2>
<span style="color: #222222"><span style="font-family: Helvetica"><span><strong>When energy fails:
Edema, heart failure, hypertension, sarcopenia, etc. </strong></span></span></span>
</h2>
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<span style="color: #222222"><span style="font-family: Helvetica"><span>More than 100 years ago the idea of
a morphogenetic field was proposed by A.G. Gurwitsch, as a way to explain the orderly movements
of cells in embryos and growing tissues, and to understand the principles that cause cells to
change appropriately when their location in the organism changes. For 30 years, the concept
guided research in embryology, but also led to important discoveries in the biology of cancer,
aging, wound repair, and other important areas. But by the late 1940s, a more abstract approach
to biology, based on the gene doctrine of Mendel and Weismann, took charge of academic and
governmental biological research. This ideology at first said that organisms are determined by
unchanging units of inheritance, "genes," and later when genes were found to be susceptible to
mutation, the changes were said to be always random. The Central Dogma of the ideology was that
any meaningful, adaptive changes that occur in an organism can't influence the genes. For many
years, adaptive changes were said to be nothing but changes in the size or function of existing
cells, because the cells of the major organs of the body were supposed to be created before
birth, or in infancy. </span></span></span>
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<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Besides the purely ideological
commitment to the theory of genes, there were other influences that contributed to the culture
of Molecular Biology. People learned histology from slides or pictures made by killing,
hardening, dehydrating, and slicing parts of organisms. Biochemists studied the chemistry of
life mainly by grinding cells or tissues, and extracting water soluble materials to study the
actions of enzymes on various materials. These unrealistic artifacts filled the textbooks and
the minds of generations of biologists and physicians. The culture of molecular biology used
these artifacts to create theories of embryology and physiology, and holistic ideas such as the
developmental field were disregarded.</span></span></span>
</blockquote>
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<span style="color: #222222"><span style="font-family: Helvetica"><span>The mental image of a living
organism that has been created by that culture is simply wrong. The concept of a developmental
field is essential for understanding embryology, because things that exist on a scale bigger
than molecules and cells govern the functions of the molecules and cells, and the principles of
embryology don't arbitrarily stop operating at birth, but can be seen to continue operating
during maturity and aging. The interactions of cells with their environment are different at
different stages of life, but there are commonalities that are extremely important.</span></span
></span>
</blockquote>
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<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The processes that govern the
pregnant woman's blood circulation, in sustaining the development of a fetus, are very similar
to the processes that govern anyone's blood circulation, providing for the maintenance and
renewal of all the body's organs. The common problems of pregnancy involving the circulatory
system can provide insights into the problems of the various organs that have been the focus of
the medical specialties, and to some basic medical issues, including aging, obesity, and
inflammation.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The development of a fertilized egg
into an embryo consumes energy at a very high rate, and the way the embryo develops depends on a
continuously adequate supply of oxygen and sugar, and other nutrients. The intense flow of
energy through each stage of a developing structure shapes the following stage. The necessary
energy and materials are provided abundantly by the mother's blood. When the development has
advanced far enough to make life possible outside the uterus, energy will be used more slowly,
for growth, maintenance, and renewal of tissues. </span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Failure to renew cells and tissues
leads to the loss of function and substance. Bones and muscles get weaker and smaller with
aging. Diminished bone substance, osteopenia, is paralleled, at roughly the same rate, by the
progressive loss of muscle mass, sarcopenia (or myopenia). The structure of aging tissue
changes, with collagen tending to fill the spaces left by the disappearing cells. It's also
common for fat cells to increase, as muscle cells disappear.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>When conditions are ideal, as during
healthy development in the uterus, tissue damage is corrected by the multiplication of cells to
replace any that were lost. But when conditions are less perfect, injuries are imperfectly
repaired, usually with highly collagenous scar tissue bridging the area that was destroyed.
During this imperfect repair, there is inflammation, which apparently exists to the extent that
the substances needed for regeneration are lacking. For example, when oxygen is lacking, lactic
acid is likely to be produced, along with increases of pro-inflammatory regulators such as
histamine and serotonin, leading to the loss of many important proteins and functions, and the
over-production of collagen instead.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Since cellular renewal of tissues,
in a healthy individual, is a constant process, we can think of the metabolic rate of a healthy
adult as just what is needed to sustain this constant, limited sort of regeneration, but not
quite intense enough to produce scarless healing of a wound (without special
intervention).</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>If something reduces the systemic
ability to produce energy, there will be a gap between the available energy and the energy
needed for the constant turnover of cells in each tissue and organ, and a generalized
inflammation will develop. The replacement of cells will be slowed, and the organism will
mobilize the processes used for producing scar tissue, producing an excess of collagen, filling
the spaces left by the lost cells.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>We are susceptible to many things
that interfere with energy production---the substitution of iron for copper in the respiratory
enzyme, the absorption of endotoxin, the accumulation of PUFA, a deficiency of thyroid hormone,
the formation of increased amounts of nitric oxide, serotonin, and histamine, etc. Different
environments will condition the way the defensive mechanisms of inflammation are
produced. </span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Toxemia of pregnancy, or
preeclampsia, is a state of generalized inflammation, and some of the causes and remedies are
known. Despite the predominance of crazy genetic theories of preeclampsia in 20th century
medical literature, there was clear evidence (reviewed by Tom Brewer, Douglas Shanklin, and Jay
Hodin) that it was caused by malnutrition, and that it could be cured by adequate protein, salt,
and calcium. </span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The old medical practice of
restricting salt intake during pregnancy was an important factor in causing it, so it's
interesting to look at the effects of salt restriction as a treatment for hypertension.</span
></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The pregnant woman's blood volume
expands, to permit the supply of energy to match the needs of the embryo. If the blood volume
doesn't increase, or if it decreases, as in pregnancy toxemia, her blood pressure will increase.
Typically, the decrease of blood volume is accompanied by an increase in the extracellular
fluid, edema, resulting from leakage of fluid through the walls of the capillaries, and albumin
appears in the urine as it leaks through the capillaries in the kidneys. The amount of blood
pumped by the heart, however, is increased in toxemia (Hamilton, 1952), showing that the
increased blood pressure is at least partially compensating for the smaller volume of
blood. </span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>A similar situation, <strong
>reduced blood volume and edema, can be seen (Tarazi, 1976) in "essential hypertension," the
"unexplained" hi</strong>gh blood pressure that occurs more often with increasing age and
obesity. At the beginning of "essential hypertension," the amount of blood pumped is usually
greater than normal.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>In both situations, preeclampsia and
essential hypertension, there is an increased amount of aldosterone, an adrenal steroid which
allows the kidneys to retain sodium, and to lose potassium and ammonium instead. A restriction
of salt in the diet causes more aldosterone to be produced, and increased salt in the diet
causes aldosterone to decrease. One effect of aldosterone is to increase the production of a
substance called vascular endothelial growth factor, VEGF, or vascular permeability factor,
which causes capillaries to become leaky, and causes new blood vessels to grow.</span></span
></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>While <strong>increased salt in
the diet tends to lower both aldosterone and VEGF, reducing the leakiness of blood
vessels, </strong>sodium also has a direct effect that tends to prevent the leakage of
water and albumin out of the blood vessels, helping to maintain the blood volume which is needed
to perfuse the kidneys, preventing them from producing signals to increase blood pressure and
aldosterone. There is a large amount of albumin in the blood serum, and sodium ions associate
with the negative electrical charges on the albumin molecule. This association causes the
complex of albumin and sodium to attract a large amount of water, that is to exert osmotic or
oncotic pressure. This oncotic pressure causes any excess extracellular water to be attracted
into the blood vessels, preventing edema while maintaining the blood volume. When there is too
little sodium, the albumin molecule itself easily leaves the blood stream along with the
water.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Instead of considering the
significance of sodium's effects on albumin, aldosterone, and VEGF, textbooks have often talked
about the factors that "pump" sodium, and factors that specifically regulate the movement of
water. Experiments in which an excess of aldosterone is combined with a high salt intake produce
increased blood pressure, and--by invoking various genes--salt is said to cause hypertension in
certain people. This reasoning is hardly different from the reasoning of the drug companies in
the 1950s who said that since women with toxemia have hypertension and edema, they should be
treated with a diuretic and a low salt diet, to eliminate water and to reduce blood
pressure.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The physiological loss of sodium
occurs when energy metabolism fails, as in<strong>diabetes, hypothyroidism, hyperestrogenism,
and starvation. </strong>What these conditions have in common is an increased level of
free fatty acids in the blood. Increased free fatty acids impair the use of glucose. The
consumption of carbohydrate, like an increase of thyroid hormone, insulin, or progesterone,
increases the retention of sodium; fructose is the most effective carbohydrate (Rebello, et al.,
1983). </span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The loss of sodium is often
accompanied by the retention of water, reducing the osmotic pressure of the body fluids. The
leakiness of blood vessels allows the extracellular fluid volume to increase, as understood in
the standard definition of edema. However, when this fluid is hypo-osmotic, it will enter cells,
causing them to swell. Cell swelling excites cells (Ayus, et al., 2008; Baxter, et al., 1991),
and can kill them if they are unable to produce enough energy to restore their original volume,
by measures including the excretion of amino acids and potassium. Both low sodium
(hyponatremia) and low osmotic pressure stimulate the adrenergic nervous system.</span></span
></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The increase of adrenalin,f caused
by a deficiency of sodium, is one of the factors that can increase blood pressure; if the
tissues's glycogen stores are depleted, the adrenalin will mobilize free fatty acids from the
tissues, which tends to inhibit energy production from glucose, and to increase leakiness. After
I had read Tom Brewer's work on preventing or curing preeclampsia with added salt, I realized
that the premenstrual syndrome involved some of the features of preeclampsia (edema, insomnia,
cramps, hypertension, salt craving), so I suggested to a friend that she might try salting her
food to taste, instead of trying to restrict salt to "prevent edema." She immediately noticed
that it prevented her monthly edema problem. For several years, all the women who tried it had
similarly good results, and often mentioned that their sleep improved. I mentioned this to
several people with sleep problems, and regardless of age, their sleep improved when they ate as
much salt as they wanted. Around that time, several studies had shown that salt restriction
increases adrenalin, and one study showed that most old people on a low sodium diet suffered
from insomnia, and had unusually high adrenalin. When they ate a normal amount of salt, their
adrenalin was normalized, and they slept better.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>It's very common for physicians who
are aware of progesterone's "anti-aldosterone" activity to think that both estrogen and
progesterone are responsible for the increased risk of sodium loss in women, especially during
pregnancy, but Hans Selye demonstrated that progesterone will normalize sodium retention even
when there is no aldosterone at all, following removal of the adrenal glands. It is estrogen
which is responsible for the dangerous loss of sodium. </span
></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The ratio of estrogen to
progesterone--regardless of age or gender--is an important factor in regulating minerals and
water, cell energy metabolism, and blood pressure. The ratios of many other regulatory
substances (including serotonin/dopamine, glucagon/insulin, and
aldosterone/cortisol+progesterone) vary according to the quality of the individual's level of
adaptation to the environment. Improving the environment can shift the ratio in the direction of
restoration, rather than mere survival.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Gershom Zajicek and his colleagues
have demonstrated an organized renewal of tissues, in which new cells are born with the division
of stem cells, and "stream" away from their origin as they mature, and finally are shed or
dissolved. A few studies have demonstrated a similar kind of migration of new cells in the brain
(Eriksson, et al., 1998; Gould, et al., 1999), a process which differs by the absence of
systematic dissolution of mature brain cells. While Zajicek has demonstrated the conversion of
one kind of cell, such as a pancreatic ductal epithelial or acinar cell into insulin-secreting
beta cells, other researchers have shown that after injury to the pancreas beta cells can be
formed from glucagon-secreting alpha cells, as well as from other beta cells. </span></span
></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Stress, increasing the need for
energy, increases the formation of cortisol and free fatty acids when glucose isn't available,
and those--while they provide alternative sources of energy--interfere with the ability to
produce energy from glucose. Free fatty acids and cortisol can cause the insulin-secreting beta
cells to die. Glucose, and insulin which allows glucose to be used for energy production, while
it lowers the formation of free fatty acids, promotes the regeneration of the beta-cells.
Although several research groups have demonstrated the important role of glucose in regeneration
of the pancreas, and many other groups have demonstrated the destructive effect of free fatty
acids on the beta cells, the mainstream medical culture still claims that "sugar causes
diabetes."</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>In the adrenal glands, renewing
cells stream from the capsule on the surface of the gland toward the center of the gland. The
first cells to be produced in a regenerating gland are those that produce aldosterone, the next
in the stream are the cortisol producing cells, and the last to be formed are the cells that
produce the sex hormones, the androgens including DHEA, and progesterone. In aging, after the
age of thirty, the renewal slows, but the dissolution of the sex hormone zone continues, so the
proportion shifts, increasing the ratio of the aldosterone and cortisol producing cells to the
layer that produces the protective androgens and progesterone (Parker, et al., 1997).</span
></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Even before aldosterone was
identified, progesterone's role in regulating the salts, water, and energy metabolism was known,
and after the functions of aldosterone were identified, progesterone was found to protect
against its harmful effects, as it protects against an excess of cortisol, estrogen, or the
androgens. New anti-aldosterone drugs are available that are effective for treating hypertension
and heart failure, and their similarity to progesterone is recognized.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>While stress typically causes the
adrenal glands to produce cortisol, extreme stress, as described by Hans Selye, damages the
adrenal cortex, and can cause the cells to die, leading to the death of the animal. There is
evidence that it is the breakdown of unsaturated fatty acids that causes damage to the adrenal
cortex in extreme stress. Although many factors influence the production of the adrenal
steroids, arachidonic acid, even without being converted to prostaglandins, is an important
activator of aldosterone synthesis. Adrenalin, produced in response to a lack of glucose,
liberates free fatty acids from the tissues, so when the tissues contain large amounts of the
polyunsaturated fatty acids, the production of aldosterone will be greater than it would be
otherwise. </span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The continuing accumulation of
polyunsaturated fats in the tissues is undoubtedly important in the changing relationship
between the pancreas and the adrenal glands in aging. Aspirin, which is antilipolytic,
decreasing the release of free fatty acids, as well as inhibiting their conversion to
prostaglandins, lowers the production of stress-induced aldosterone, and helps to lower blood
pressure, if it's taken in the evening, to prevent the increase of free fatty acids during the
night. Aspirin increases insulin sensitivity. A low salt diet increases the free fatty acids,
leading to insulin resistance, increasing free fatty acids in the blood, and contributing to
atherosclerosis (Prada, et al., 2000; Mrnka, et al., 2000; Catanozi, et al., 2003; Garg, et al.,
2011).</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>The same factors that support or
interfere with cellular renewal in the pancreas and adrenal glands have similar effects in the
bones, skin, skeletal and heart muscle, nervous system, liver, and other organs. In every case,
the local circulation of blood is influenced by both local and systemic factors. The loss of
control over the water in the body is the result of energy failure, and hypertension is one of
the adaptations that helps to preserve or restore energy production. </span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Lowering inflammation and the
associated excess of free fatty acids in the blood, and improving the ability to oxidize
glucose, will lower blood pressure while improving tissue renewal, but lowering blood pressure
without improving energy production and use will create new problems or intensify existing
problems. After 40 years the medical profession quietly retreated from their catastrophic
approach to pregnancy toxemia, but in the more general problem of essential hypertension, the
mistaken ideology is being preserved, even as less harmful treatments are introduced. That
ideology prevents a comprehensive and rational approach to the problems of stress and
aging.</span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222">
<span style="font-family: Helvetica"><span><strong><h3>REFERENCES</h3></strong
></span></span></span>
</blockquote>
<blockquote></blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Med Sci Monit. 2002
Jul;8(7):CR473-7. <strong>Effect of renin-angiotensin system activation by dietary sodium
restriction and upright position on plasma leptin concentration in patients with essential
hypertension. </strong>Adamczak M, Kokot F, Chudek J, Wiecek A.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Obesity (Silver Spring). 2006
Sep;14(9):1571-8. <strong>Associations between aortic calcification and components of body
composition in elderly men. </strong>Alexandersen P, Tankó LB, Bagger YZ, Jespersen J,
Skouby SO, Christiansen C.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Am J Physiol Renal Physiol. 2008
Sep;295(3):F619-24. <strong>Brain cell volume regulation in hyponatremia: role of sex, age,
vasopressin, and hypoxia. </strong>Ayus JC, Achinger SG, Arieff A. </span
></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Neurochem Res 1991
Mar;16(3):269-78. <strong>Alterations of GABA metabolism and seizure susceptibility in the
substantia nigra of the kindled rat acclimating to changes in osmotic state.</strong
> Baxter CF, Oh CC, Wasterlain CG, Ozaki LK, Baldwin RA.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Diabetes. 2012
Mar;61(3):560-1. <strong>Does inhibition of beta-cell proliferation by free fatty acid in
mice explain the progressive failure of insulin secretion in type 2 diabetes? </strong
>Boden G.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>BJOG. 2004
Sep;111(9):1020-2. <strong>Severe hyponatraemia and pre-eclampsia. </strong>Burrell C,
de Swiet M.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Stem Cells. 2010
Sep;28(9):1630-8. <strong>Pancreatic β-cell neogenesis by direct conversion from mature
α-cells. </strong>Chung CH, Hao E, Piran R, Keinan E, Levine F.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Eur Respir J Suppl. 2003
Nov;46:33s-40s. <strong>Fluid homeostasis in chronic obstructive lung
disease. </strong>de Leeuw PW, Dees A.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Trends Endocrinol Metab. 2011
Jan;22(1):34-43. <strong>Beta-cell regeneration: the pancreatic intrinsic faculty.</strong
> Desgraz R, Bonal C, Herrera PL.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Am J Physiol. 1993 May;264(5 Pt
1):E730-4. <strong>Effect of sodium intake on insulin sensitivity.</strong>Donovan DS,
Solomon CG, Seely EW, Williams GH, Simonson DC.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Nat Med. Novemeber 4,
1998. </span></span></span>
<span style="color: #222222"><span style="font-family: Helvetica"><span><strong>Neurogenesis in the adult
human hippocampus.</strong></span></span></span>
<span style="color: #222222"><span style="font-family: Helvetica"><span> Eriksson, PS., </span
></span></span>
<a href="http://et.al/" target="_blank"><span style="color: #1155cc"><span
style="font-family: Helvetica"
><span>et.al</span></span></span></a>
<span style="color: #222222"><span style="font-family: Helvetica"><span>.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Exp Med. 1996 May
1;183(5):1981-6. <strong>Vesiculo-vacuolar organelles and the regulation of venule
permeability to macromolecules by vascular permeability factor, histamine, and
serotonin. </strong>Feng D, Nagy JA, Hipp J, Dvorak HF, Dvorak AM.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Metabolism. 2011 Jul;60(7):965-8.
Epub 2010 Oct 30. <strong>Low-salt diet increases insulin resistance in healthy
subjects.</strong> Garg R, Williams GH, Hurwitz S, Brown NJ, Hopkins PN, Adler
GK.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Curr Opin Endocrinol Diabetes Obes.
2012 Jun;19(3):168-75. <strong>Role of mineralocorticoid receptor in insulin
resistance. </strong>Garg R, Adler GK.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Clin Endocrinol Metab. 1991
Nov;73(5):975-81. <strong>Effects of sodium supplementation during energy restriction on
plasma norepinephrine levels in obese women. </strong>Gougeon R, Mitchell TH, Lariviere
F, Abraham G, Montambault M, Marliss EB.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Science. October 15,
1999. </span></span></span>
<span style="color: #222222"><span style="font-family: Helvetica"><span><strong>Neurogenesis in the
Neocortex of Adult Primates.</strong></span></span></span>
<span style="color: #222222"><span style="font-family: Helvetica"><span> Gould, E., </span></span
></span>
<a href="http://et.al/" target="_blank"><span style="color: #1155cc"><span
style="font-family: Helvetica"
><span>et.al</span></span></span></a>
<span style="color: #222222"><span style="font-family: Helvetica"><span>.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Renin Angiotensin Aldosterone
Syst. 2011 Dec;12(4):430-9. <strong>Study of the mechanisms of aldosterone prothrombotic
effect in rats.</strong> Gromotowicz A, Szemraj J, Stankiewicz A, Zakrzeska A, Mantur
M, Jaroszewicz E, Rogowski F, Chabielska E.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Postepy Hig Med Dosw (Online). 2010
Oct 18;64:471-81. <strong>[Prothrombotic aldosterone action--a new side of the
hormone]. </strong>[Article in Polish] Gromotowicz A, Osmolska U, Mantur M, Szoka P,
Zakrzeska A, Szemraj J, Chabielska E.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Semin Nephrol 15: 593-602,
1995. <strong>Mechanisms of calcium's effects on blood pressure.</strong>Hatton DC, Que Y,
McCarron DA.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Ugeskr Laeger. 1960 Feb
25;122:244-51. <strong>[The aldosterone-antagonistic effect of progesterone. A preliminary
note on the effects of progesterone on 2 patients with liver cirrhosis].</strong
> [Article in Danish] Hempel-Jorgensen P, Eilersen P.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Obstetrical &
Gynecological Survey: 7(3): 347, 1952. <strong>Cardiac output in hypertensive toxaemias of
pregnancy, </strong>Hamilton HFH.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Am J Obstet Gynecol. 1998
Nov;179(5):1312-6. <strong>Dilutional hyponatremia in pre-eclampsia.</strong>Hayslett JP,
Katz DL, Knudson JM.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Clin Invest. 1970
Jun;49(6):1224-36. <strong>Studies on the exaggerated natriuretic response to a saline
infusion in the hypothyroid rat. </strong>Holme<strong>s</strong> EW Jr, DiScala
VA.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Vnitr Lek. 2011
Dec;57(12):1012-6. <strong>[Aldosterone as an endogenous cardiovascular toxin and the
options for its therapeutic management]. </strong>[Article in Czech] Horky K.</span
></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Atherosclerosis. 1990
Oct;84(2-3):229-37. <strong>Fish oil produces an atherogenic lipid profile in hypertensive
men.</strong> Hughes GS, Ringer TV, Watts KC, DeLoof MJ, Francom SF, Spillers CR.</span
></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Eur J Appl Physiol Occup Physiol.
1995;72(1-2):165-9. <strong>Arterial diameter during central volume depletion in
humans. </strong>Iversen HK, Madsen P, Matzen S, Secher NH.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Proceedings of the National Academy
of Sciences, May 11, 1999. <strong>Continuatoin of neurogenesis in the hippocampus of the
adult macaque monkey.</strong> Kornack, D. and P. Rakic.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Acta Pathol Microbiol Scand A. 1975
Nov;83(6):661-8. <strong>The effect of angiotensin infusion, sodium loading and sodium
restriction on the renal and cardiac adrenergic nerves.</strong>Ljungqvist A.</span></span
></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Clin Hypertens (Greenwich). 2002
May-Jun;4(3):173-80. <strong>Moderate sodium restriction enhances the pressor response to
hyperlipidemia in obese, hypertensive patients. </strong>Lopes HF, Stojiljkovic MP,
Zhang D, Goodfriend TL, Egan BM.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Am Coll Nutr 17(1): 97-98,
1998. <strong>Importance of dietary calcium in hypertension.</strong> McCarron,
DA.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Science 217:267-269,
1982. <strong>Dietary calcium in human hypertension</strong>. McCarron DA, Morris C, Cole
C.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Exp Neurol. 2012
Mar;234(1):200-7. <strong>Stress and corticosteroid modulation of seizures and synaptic
inhibition in the hippocampus.</strong> Maggio N, Segal M.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Exp Clin Endocrinol Diabetes. 2009
Jun;117(6):274-82. <strong>Roles of inhibitors of poly(ADP-ribose) polymerase in protecting
rat RINm5F cell line against free fatty acid-induced apoptosis. </strong>Mao X, Wang S,
Pan Y, He B, Chen J, Jiang H, Zeng Q, Xu X.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Hum Hypertens. 1988
Mar;1(4):293-8. <strong>Changes in plasma lipids and uric acid with sodium loading and
sodium depletion in patients with essential hypertension. </strong>Masugi F, Ogihara T,
Hashizume K, Hasegawa T, Sakaguchi K, Kumahara Y.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Jpn Circ J. 1977
Mar;41(3):228-36. <strong>Studies on the role of sympathetic nervous system in the
mechanism of essential hypertension. </strong>Miyahara M, Iimura O, Shoji T, Okada
T.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Am J Hypertens 5: 1S-42S,
1992. <strong>A comprehensive review of the salt and blood pressure
relationship. </strong>Muntzel, Drueke T.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Atherosclerosis. 2008
Oct;200(2):410-6. <strong>Dietary salt restriction increases plasma lipoprotein and
inflammatory marker concentrations in hypertensive patients. </strong>Nakandakare ER,
Charf AM, Santos FC, Nunes VS, Ortega K, Lottenberg AM, Mion D Jr, Nakano T, Nakajima K, D'Amico
EA, Catanozi S, Passarelli M, Quintao EC.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Curr Diabetes Rev. 2010
May;6(3):184-90. <strong>Production of pancreatic beta-cells from stem cells. </strong
>Noguchi H.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Membr Biol. 2001 Dec
1;184(3):305-11. <strong>Intracellular pH as a regulator of Na + transport.</strong>Palmer
LG.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Clin Endocrinol Metab. 1997
Nov;82(11): 3898-901. <strong>Aging alters zonation in the adrenal cortex of men.</strong
> Parker CR Jr, Mixon RL, Brissie RM, Grizzle WE.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Card Fail. 2009
Dec;15(10):864-73. <strong>Long-term effects of dietary sodium intake on cytokines and
neurohormonal activation in patients with recently compensated congestive heart
failure. </strong>Parrinello G, Di Pasquale P, Licata G, Torres D, Giammanco M, Fasullo
S, Mezzero M, Paterna S.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Kidney Int. 2004
Dec;66(6):2155-66. <strong>High calcium diet down-regulates kidney angiotensin-converting
enzyme in experimental renal failure.</strong> Porsti I, Fan M, Koobi P, Jolma P,
Kalliovalkama J, Vehmas TI, Helin H, Holthofer H, Mervaala E, Nyman T, Tikkanen I.</span></span
></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Eur J Appl Physiol. 2003
Apr;89(2):177-83. <strong>The influence of aspirin on exercise-induced changes in
adrenocorticotrophic hormone (ACTH), cortisol and aldosterone (ALD) concentrations.</strong
> Przybylowski J, Obodynski K, Lewicki C, Kuzniar J, Zaborniak S, Drozd S, Czarny W,
Garmulewicz M.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Free Radic Biol Med. 2011 Dec
1;51(11):1996-2006. <strong>Aldosterone increases kidney tubule cell oxidants through
calcium-mediated activation of NADPH oxidase and nitric oxide synthase. </strong
>Queisser N, Schupp N, Stopper H, Schinzel R, Oteiza PI. "Chronic hyperaldosteronism has been
associated with an increased cancer risk."</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Obstet Gynaecol. 2006
Oct;26(7):695-6. <strong>Pre-eclampsia and hyponatraemia.</strong> Ray CD, Shenoy JV,
Hare AA.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Am J Clin Nutr. 1983
Jul;38(1):84-94. <strong>Short-term effects of various sugars on antinatriuresis and blood
pressure changes in normotensive young men.</strong> Rebello T, Hodges RE, Smith
JL.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Klin Wochenschr. 1991;69 Suppl
25:51-7. <strong>Short-term dietary sodium restriction increases serum lipids and insulin
in salt-sensitive and salt-resistant normotensive adults. </strong>Ruppert M, Diehl J,
Kolloch R, Overlack A, Kraft K, Gobel B, Hittel N, Stumpe KO.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Hypertension. 2007
Oct;50(4):773-9. <strong>Pregnant rats treated with a serotonin precursor have reduced
fetal weight and lower plasma volume and kallikrein levels.</strong> Salas SP, Giacaman
A, Romero W, Downey P, Aranda E, Mezzano D, Vio CP.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Bioessays. 2010
Oct;32(10):881-4. <strong>A new paradigm in cell therapy for diabetes: turning pancreatic
alpha-cells into beta-cells. </strong>Sangan CB, Tosh D.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Arq Bras Endocrinol Metabol. 2009
Jul;53(5):608-16. <strong>[Sodium intake and metabolic syndrome: a systematic
review].</strong> [Article in Portuguese] Sarno F, Jaime PC, Ferreira SR, Monteiro
CA.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Brain Res. 2001 Sep
21;913(2):149-55. <strong>Changes in rat cerebral blood volume due to modulation of the
5-HT(1A) receptor measured with susceptibility enhanced contrast MRI.</strong>Scanley BE,
Kennan RP, Gore JC.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Hypertens. 1993
Dec;11(12):1381-6. <strong>Effect of dietary salt restriction on urinary serotonin and
5-hydroxyindoleacetic acid excretion in man.</strong> Sharma AM, Schorr U, Thiede HM,
Distler A. <strong>"During the low-salt diet, 24-h urinary excretion of serotonin increased
by 42%, accompanied by a 52% rise in the excretion of 5-HIAA. Salt restriction also
increased noradrenaline excretion by 77% and VMA excretion by 40%." "Salt restriction
stimulates the serotonergic system in man." </strong></span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Lab Clin Med. 1989
Oct;114(4):338-48. <strong>Calcium and hypertension. </strong>Sowers JR, Zemel MB,
Standley PR, Zemel PC.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Endocrinology. 1988
Aug;123(2):975-80. <strong>Effects of tocopherol depletion on the regional differences in
adrenal microsomal lipid peroxidation and steroid metabolism.</strong> Staats DA, Lohr
DP, Colby HD.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Hypertension. 2009
Sep;54(3):552-7. <strong>Role of mineralocorticoid receptor on experimental cerebral
aneurysms in rats.</strong> Tada Y, Kitazato KT, Tamura T, Yagi K, Shimada K, Kinouchi
T, Satomi J, Nagahiro S.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Circ Res. 1976 Juh;38(6 Suppl
2):73-83. <strong>Hemodynamic role of extracellular fluid in hypertension. </strong
>Tarazi RC. "Plasma volume is usually lower in patients with essential hypertension than in
normal subjects." Essential hypertensives as a group have low plasma to interstitial fluid
volume ratio...."</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Med Sci (Paris). 2010
Nov;26(11):906-9. <strong>[Conversion of adult pancreatic alpha-cells to beta-cells in
diabetic mice].</strong> [Article in French] Thorel F, Herrera PL.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Eur J Neurosci. 2004
Feb;19(4):916-24. <strong>Depolarization, exocytosis and amino acid release evoked by
hyposmolarity from cortical synaptosomes.</strong> Tuz K, Pena-Segura C, Franco R,
Pasantes-Morales H.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Eur J Neurosci. 2005
Oct;22(7):1636-42. <strong>Hyposmolarity evokes norepinephrine efflux from synaptosomes by
a depolarization- and Ca2+ -dependent exocytotic mechanism.</strong> Tuz K,
Pasantes-Morales H.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Gynecol Endocrinol. 2005
Nov;21(5):243-7. <strong>Drospirenone in the treatment of severe premenstrual cerebral
edema in a woman with antiphospholipid syndrome, lateral sinus thrombosis, situs inversus
and epileptic seizures. </strong>Vujovic S, Zidverc J, Stojanovic M, Penezic Z, Ivovic
M, Dukic V, Drezgic M.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Hypertens. 1988
Jun;6(6):471-9. <strong>Mechanism of action of ketanserin: studies on cardiovascular
reactivity in essential and diabetes-associated hypertension. </strong>Waser M, Ziegler
WH, Beretta-Piccoli C. "Ketanserin treatment administered over a period of 8 weeks, decreased
arterial pressure in patients with essential hypertension and, to a lesser extent, in diabetics,
but not in normal subjects."</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Aust J Exp Biol Med Sci. 1976
Feb;54(1):71-8. <strong>Regulation of aldosterone in the guinea-pig--effect of oestrus
cycle, pregnancy and sodium status.</strong> Whipp GT, Wintour EM, Coghlan JP, Scoggins
BA. Compared with a moderate Na intake, salt loading suppressed aldosterone levels and Na
restriction raised them.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J Clin Invest. 1972
Oct;51(10):2645-52. <strong>Studies of the control of plasma aldosterone concentration in
normal man. 3. Response to sodium chloride infusion. </strong>Williams GH, Tuck ML,
Rose LI, Dluhy RG, Underwood RH.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Diabet. Research. 13:121-125,
1990. <strong>Streaming Pancreas : Islet cell kinetics.</strong> Zajicek G, Arber N.
Schwartz-Arad D, Ariel I.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Path. Res. Pract.
188:410-412,1992. <strong>Time dimension in histopathology,</strong> Zajicek
G </span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Zajicek G. <strong>Streaming
Organism: The Tissue Automat. </strong>in: Computing with Biological Metaphors. Ed. R.
Paton.Chapman & Hall London, 1994.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Methods of Inform. Med.
26:1-2,1987. <strong>The time dimension in histology. </strong>Zajicek G.</span
></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>Liver 5:293-300,1985. <strong
>The streaming liver.</strong> Zajicek,G.;Oren,R.;Weinreb,Jr. </span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J. Endocr. 111:
447-482,1986. <strong>The streaming adrenal cortex: direct evidence of centripetal
migration of adrenocytes by estimation of cell turnover rate.</strong> Zajicek G.,Ariel
I.,Arber N.</span></span></span>
</blockquote>
<blockquote>
<span style="color: #222222"><span style="font-family: Helvetica"><span>J. Pharm Pharmacol. 2002
Apr;54(4):577-82. <strong>Non-steroidal anti-inflammatory drugs inhibit epinephrine- and
cAMP-mediated lipolysis in isolated rat adipocytes.</strong> PM de Zentella,
Vazquez-Meza H, Pina-Zentella G, Pimentel L, Pina E, </span></span></span>
</blockquote>
<blockquote></blockquote>
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