Abstract
We used the isolated rabbit aorta to examine the mechanisms that mediate the known vasodilatation induced by 17-beta-estradiol. Our results suggest that nitric oxide (NO), the inhibition of Ca2+ release from intracellular stores through the IP3 pathway and Ca2+ influx through potential-dependent calcium channels (PDCs) seem to be involved. Prostaglandins and adrenergic beta receptors do not influx, intracellular Ca2+ release, NO, cyclic guanine monophosphate (cGMP), prostaglandins and adrenergic beta receptors.
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