Abstract
The relaxation of coronary arteries by estrogens in the coronary vascular beds of naive and hypertensive rats has been well described. However, little is known about this action in gonadectomized rats. We investigated the effect of 17-ß-estradiol (E2) in coronary arteries from gonadectomized rats, as well as the contributions of endothelium-derived factors and potassium channels. Eight-week-old female and male Wistar rats weighing 220-300 g were divided into sham-operated and gonadectomized groups (n=9−12 animals per group). The baseline coronary perfusion pressure (CPP) was determined, and the vasoactive effects of 10 μM E2 were assessed by bolus administration before and after endothelium denudation or by perfusion with NG-nitro-L-arginine methyl ester (L-NAME), indomethacin, clotrimazole, L-NAME plus indomethacin, L-NAME plus clotrimazole or tetraethylammonium (TEA). The CPP differed significantly between the female and sham-operated male animals. Gonadectomy reduced the CPP only in female rats. Differences in E2-induced relaxation were observed between the female and male animals, but male castration did not alter this response. For both sexes, the relaxation response to E2 was, at least partly, endothelium-dependent. The response to E2 was reduced only in the sham-operated female rats treated with L-NAME. However, in the presence of indomethacin, clotrimazole, L-NAME plus indomethacin or L-NAME plus clotrimazole, or TEA, the E2 response was significantly reduced in all groups. These results highlight the importance of prostacyclin, endothelium-derived hyperpolarizing factor, and potassium channels in the relaxation response of coronary arteries to E2 in all groups, whereas nitric oxide may have had an important role only in the sham-operated female group.
Highlights
Sex differences in the incidence of cardiovascular diseases (CVDs), such as hypertension and coronary artery disease, have been reported
The risk of CVDs is greater in postmenopausal women compared to premenopausal women, which suggests that there are vascular benefits of estrogens and that the decrease in plasma levels of estrogens during menopause may contribute to this risk [2,3]
These results suggest that after treatment with sodium deoxycholate, the ability of coronary endothelial cells to produce relaxation factors is reduced, whereas the ability of vascular smooth muscle cells to respond to sodium nitrite remains unchanged
Summary
Sex differences in the incidence of cardiovascular diseases (CVDs), such as hypertension and coronary artery disease, have been reported. The risk of CVDs is greater in postmenopausal women compared to premenopausal women, which suggests that there are vascular benefits of estrogens and that the decrease in plasma levels of estrogens during menopause may contribute to this risk [2,3]. The roles of female sex steroids in mediating or protecting against CVDs are controversial [4]. Estrogens may play an important role in regulating ion channels in vascular smooth muscle cells [8]. Many other beneficial vascular effects of estrogens have been suggested, including anti-proliferative effects on vascular smooth muscle cells [9], and composition modifications of circulating lipoproteins (e.g., decrease low-density lipoprotein cholesterol and increase high-density lipoprotein cholesterol) [10]. Estrogens directly inhibit cardiovascular L-type Ca2+ channels [11]
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Schedule a callMore From: Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
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