ROLE OF CALCIUM CHANNEL ANTAGONISM IN VASODILATOR EFFECTS OF 17-ESTRADIOL

Abstract

Cardiovascular events are less prevalent in premenopausal women and women receiving oestrogen replacement than in postmenopausal women or men. The mechanisms that mediate this apparent benefit are still unclear. Suggested mechanisms include coronary vasodilatation. The vasodilator activity is mainly suggested to be mediated through action on calcium ion channel antagonism and nitric oxide production from the vascular endothelium. This study was aimed to evaluate the extent of role of calcium channel blockade underlying the vasodilator action of the 17ï¢-estradiol. Materials and Methods: 32 male albino rats were divided into three groups. In group I, tissue was challenged with serial dilutions of norepinephrine and standard concentration was selected producing approximately 75% of maximum vasoconstriction. In group II, tissue was challenged with verapamil and standard concentration was selected in the presence of norepinephrine mediated vasoconstriction, and in group III, tissue was challenged with serial dilution of 17ï¢-estradiol after pretreatment with verapamil the presence of norepinephrine mediated vasoconstriction. Results: Results obtained showed that vasodilator activity of both the drugs was almost similar up to 10-7 gm/ml concentration. At higher concentrations, 17ï¢-estradiol showed greater vasodilator response suggesting the possibility of presence of other mechanisms independent of calcium channel antagonism in addition to calcium channel blockade. Conclusion: Our observations suggest that vasodilator activity of 17-ï¢-estradiol is not mediated through calcium channel antagonism only. It suggests the possibility of other mechanism(s) also, underlying these cardioprotective effects in post menopausal women.