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Archivos Venezolanos de Farmacología y Terapéutica
versión impresa ISSN 0798-0264
Resumen
ROMERO V, E et al. Cambios Ontogénicos en la Reactividad Cardiovascular inducidos por los Esteroides Androgénicos. AVFT [online]. 2002, vol.21, n.1, pp.16-21. ISSN 0798-0264.
Higher epidemiological incidence of fatal cardiovascular effects in men compared to women is the subject of intense research in order to find out the role of testosterone. Cardiovascular protection provided by estrogens in postmenopausal women is 30-40% when compared to untreated ones. Some studies have found that very high doses of androgenic steroids induce an atherogenic lipid profile by increasing LDL and reducing HDL; however, other studies have shown an antiatherogenic effect. Testosterone increases monocyte adhesion to human endothelial cells and in turn they express more intensely the adhesine molecule VCAM-1. Human "ex vivo" macrophages when exposed to testosterone can uptake more avidly a charge of lipid molecules while estrogens does not show this effect. It has been found that testosterone can increase the endothelial dependent and independent vasodilatory response, and this response is antagonized by tobacco smoke exposure or by experimental hypercholesterolemia. There has been contradictory effects of testosterone in man; besides its atherogenic -induced changes, in prostate cancer men deprived of androgens, endothelial vasodilatory response improves. The experimental vasodilatory response induced by testosterone is blocked by L-NAME, which suggests it is mediated by nitric oxide synthesis. The vasodilatory action of testosterone may by also caused by potassium channels opening because this effect is antagonized by barium chloride. The ontogenic development of the endothelial vasodilatory response in rats is similar in newborns male and female rats and progresively increase until sexual maturity is reached in both sexes. On the other hand; endothelial independent vasodilation diverges in both male and female rats; it increases up to sexual maturity in males and decreases until adult life in females; this means that male rats are provided in adult life with an stronger endogenous vascular non-endothelial vasodilator mechanism. It is unknown if this mechanism operates in male men.
Palabras clave : Testosterone; Vascular reactivity; Endotelial vasodilatation; Ontogeny.












