Biomedical Bulletin

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Biomedical Bulletin
Every month a great deal of new biomedical information comes to our attention, but we can’t report on all of it, because of space limitations and our desire to do justice to our topics. With the introduction of Biomedical Bulletin last month, we’re testing the water with a different format, designed to bring you more topics while taking up less of your valuable time. Please let us know what you think, pro or con, about this new feature.

DHEA Improves Women’s Cardiovascular Function
Sex-hormone precursor has beneficial effect on blood vessels

he cardiovascular system is basically a closed-loop plumbing network, with one pump (the heart) and about 60,000 miles (yes, miles) of blood vessels. Among the most important of the many factors involved in maintaining optimal functioning of this vital system is the vascular endothelium, the layer of flat, smooth, tightly packed endothelial cells that line the insides of our blood vessels. It is here that the amino acid arginine is converted to nitric oxide, the signaling molecule that causes the underlying smooth muscle cells of our arteries to relax when needed, allowing the arteries to dilate. This vasodilation increases blood flow while keeping blood pressure under control.

Low DHEA Levels Correlate with Increased Cardiac Risk in Men

Many substances in our bloodstream affect cardiovascular function in one way or another. Among them are the catecholamines adrenaline and noradrenaline; the electrolytes sodium, potassium, calcium, and magnesium; the androgens and estrogens (male and female sex hormones, respectively); and corticosteroids such as cortisol and aldosterone. And then there is the corticosteroid DHEA (dehydroepiandrosterone), an androgen whose levels decline sharply—in both men and women—as we age (gracefully, of course).

Epidemiological studies have shown an inverse correlation between DHEA levels and the risk of cardiac mortality in men.1* It has long been known that DHEA affects cardiovascular function, and it has long been believed that its action is mediated primarily through its conversion to androgens and estrogens, for both of which it is a precursor molecule.


*There is also limited evidence for a beneficial role of DHEA in other pathological conditions, including immune system disorders (see the news brief preceding this one), malignancies, and neurological dysfunctions.2


DHEA Improves Vascular Function in Women

Now, however, there is evidence that DHEA may act independently on the vascular endothelium.2 Researchers in Australia found that DHEA significantly increased nutrient-induced cell proliferation in cultured endothelial cells from calf aortas. Significantly, it did so independently of androgen or estrogen receptors on the endothelial cell walls, meaning that it was the DHEA molecules themselves that were responsible for the effect. This suggests that there are cellular receptors specific to DHEA itself. In addition, DHEA significantly increased the expression of endothelial nitric oxide synthase, the enzyme that catalyzes the conversion of arginine to nitric oxide in the endothelial cells.

But there’s more. Following the laboratory experiments, the researchers conducted a randomized, double-blind, placebo-controlled trial with 36 healthy postmenopausal women (average age 58), in which they administered DHEA (100 mg/day) or placebo for 12 weeks. Using a standard ultrasound technique for measuring the diameter of arteries, they found that DHEA significantly increased dilation of the brachial artery (the main artery of the arm) when blood flow was restored after being temporarily restricted by a pressure cuff; by contrast, placebo had no effect on dilation.

Finally, the researchers used a laser technique for measuring subcutaneous blood flow (i.e., blood flow in the microvasculature just below the skin) in response to transcutaneous (through-the-skin) infusion of acetylcholine, which acts as a vasodilator. They found that, after 12 weeks, DHEA significantly increased the women’s blood flow in this test, compared with the baseline value established at the beginning of the study; again, placebo had no effect.

DHEA May Reduce Cardiovascular Risk

In both of the experiments just described, the researchers were able, through additional tests, to rule out nonendothelial mechanisms for DHEA’s actions, thus confirming that the effects did, indeed, occur in the endothelium of both large and small blood vessels. The authors concluded,

In summary, our findings implicate the peripheral vasculature as a potential site for DHEA action and extend our current understanding of the mechanisms by which DHEA may contribute to the amelioration of cardiovascular disease. These results suggest that DHEA and its receptor may offer possibilities for novel therapies for the management of cardiovascular risk and established cardiovascular disease.

References

  1. Alexandersen P, Haarbo J, Christiansen C. The relationship of natural androgens to coronary heart disease in males: a review. Atherosclerosis 1996; 125:1-13.
  2. Williams MRI, Dawood T, Ling S, Dai A, Lew R, Myles K, Funder JW, Sudhir K, Komesaroff PA. Dehydroepiandrosterone increases endothelial cell proliferation in vitro and improves endothelial function in vivo by mechanisms independent of androgen and estrogen receptors. J Clin Endocrinol Metab 2004;89(9):4708-15.

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