Aldosteronism & Vitamin D Deficiency

Aldosteronism & Vitamin D Deficiency
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Aldosteronism is the condition in which the adrenal glands produce too much of the hormone aldosterone. Aldosterone targets the collecting ducts in the kidneys and increases sodium and water reabsorption and the secretion of potassium. Renin, an enzyme secreted by the kidneys, is the primary regulator of aldosterone production and release. A study published in the July 15, 2002, "Journal of Clinical Investigation" reported that vitamin D suppresses renin production in animals. A study published in the June 2010 issue of the "International Journal of Clinical Chemistry" described for the first time in humans that low levels of vitamin D up-regulated the renin-angiotensin-aldosterone system. These results suggest that vitamin D also functions in the regulation of systems known to directly affect the cardiovascular system.

Renin-Angiotensin-Aldosterone System

The renin-angiotensin-aldosterone system regulates blood pressure, electrolyte balance and blood volume. Cells in the kidney respond to a decrease in blood pressure and release renin, an enzyme that processes angiotensinogen to angiotensin 1. Angiotensin 1 is converted to the potent vasoconstrictor, angiotensin 2 by another enzyme in the lungs. This causes an increase in blood pressure. Renin also acts on the adrenal gland, causing release of aldosterone, which further increases blood volume and blood pressure. In fact, many drugs that treat hypertension target the renin-angiotensin-aldosterone system.

Vitamin D Deficiency

Foods such as salmon, tuna and eggs, fortified dairy products and vitamin D3 production in the skin are the sources of vitamin D3 in humans. Vitamin D3 is converted to its active form by enzymes in the liver, kidney and cells of the immune system. The active form is called calcitriol, which is a hormone that regulates bone remodeling, calcium and phosphate levels, cell growth and also protects against pathogens. A study in the December 2008 “Journal of the American College of Cardiology” reported that vitamin D deficiency is prevalent in approximately 30 to 50 percent of the general population and because it is associated with the elevation of renin, angiotensin 2 and aldosterone levels it is a risk factor for hypertension and other cardiovascular dysfunctions.

Aldosteronism

There are two types of aldosteronism, primary aldosteronism and secondary aldosteronism. They differ in the cause of the increased production and secretion of aldosterone. A benign tumor in the adrenal glands is the usual cause of primary aldosteronism. In secondary aldosteronism the cause is related to an increase in the production of renin. A tumor in the cells that produce renin may lead to an increase in aldosterone levels. Also, because blood flow regulates renin secretion, conditions such as renal artery stenosis can increase renin and consequently aldosterone.

Evidence of Causation

There is little evidence that supports vitamin D deficiency directly causes aldosteronism. However, a case report published in the Dec. 1, 2006, "Southern Medical Journal" noted that the two conditions have occurred in an individual simultaneously. Additionally, animal studies have revealed that vitamin D increases renin levels.

Symptoms

Persons with aldosteronism can be asymptomatic or exhibit hypertension, increased thirst and urination and muscle weakness and fatigue, caused from low levels of potassium. Additionally, high aldosterone levels can cause alkalosis, a condition in which the blood pH is increased.

Hypertension

A study reported in the April 1989 “American Journal of Hypertension” did report that vitamin D supplementation reduced hypertension in patients. A May 2010 review article in the “Cleveland Clinic Journal of Medicine” noted that the physiology of vitamin D suggests it would beneficially act in patients with heart failure; however, clinical trials have not been done to assess whether vitamin D supplementation reduces mortality in patients with heart failure or that it decreases the risk of cardiovascular disease.

References

Article reviewed by M.J. Ingram Last updated on: Jul 6, 2010

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