Surgically induced deficiency of sex hormones modulates coronary vasodilation by estradiol in hypertension.

Abstract

The effect of oestrogen in hormonal dysfunction is not clear, especially in the coronary vascular bed. This study aimed at estradiol action (E2) in the coronary vascular bed from sham-operated and gonadectomized female and male spontaneously hypertensive rats (SHRs). Male and female SHRs had their mean arterial pressure (MAP) and baseline coronary perfusion pressure (CPP) determined. The effects of E2 (10μM) were evaluated in isolated hearts by in bolus infusion before and after endothelium denudation (0.25μM sodium deoxycholate) or perfusion with 100μM NG-nitro-l-arginine methyl ester (L-NAME), 2.8μM indomethacin, 0.75μM clotrimazole, L-NAME after endothelium denudation, L-NAME plus indomethacin, or 4mM tetraethylammonium (TEA). MAP was higher in males than in females, with gonadectomy increasing in females and reducing in males. CPP was higher in female group, remaining unaltered after gonadectomy. E2-induced vasorelaxation was observed in all groups, with no differences having been found between sexes even after gonadectomy. Perfusion with TEA, L-NAME, L-NAME plus indomethacin, and L-NAME after endothelium removal attenuated the relaxing response in all groups. Clotrimazole inhibited vasorelaxation only in female groups, and indomethacin did so only in gonadectomized groups. Endothelium participation was confirmed in female groups and in the gonadectomized male group. Our results indicated that the vasodilator effect of E2 was mediated by an indirect mechanism- via endothelium- as well as by direct action- via vascular smooth muscle- in both groups. The characterization of these mechanisms in coronary arteries might shed light on the functional basis of hormonal dysfunction symptoms in hypertension.