Evidence that chronic administration of 17β‐estradiol decreased the vasopressor responses in streptozotocin‐diabetic female rats (1051.9)

Abstract

In vitro studies have shown that 17β‐estradiol has beneficial effects in the cardiovascular system by activation of nitric oxide pathway. However, these effects have not been demonstrated in streptozotocin‐induced diabetic rats in the systemic vasculature in vivo. Thus, this study determined the effect of 17β‐estradiol on the vasopressor responses induced by sympathetic stimulation or i.v. injections of noradrenaline, methoxamine and B HT 933 in sham‐operated or ovariectomized, diabetic or non‐diabetic female rats. For this purpose, rats were ovariectomized or sham‐operated. One week later the animals were treated with streptozotocin (60 mg/kg, i.p.) or its vehicle. Two weeks later these rats were treated with 17β‐estradiol (10 μg/kg, s.c.) or its vehicle daily during five weeks. Then, under anaesthesia with ketamine and xylazine, the animals were pithed and prepared to measure blood pressure and heart rate. 17β‐estradiol failed to modify the vasopressor responses to: (i) sympathetic stimulation, noradrenaline, methoxamine or B HT 933 in sham‐operated non‐diabetic rats; (ii) sympathetic stimulation or B‐HT 933 in sham‐ operated diabetic rats; (iii) noradrenaline or methoxamine in ovariectomized non‐diabetic rats. In contrast, 17β‐estradiol significantly decreased the vasopressor responses to: (i) noradrenaline and methoxamine in sham‐operated diabetic rats; (ii) sympathetic stimulation or B‐HT 933 in ovariectomized non‐diabetic rats; and (iii) sympathetic stimulation, noradrenaline, methoxamine or B HT 933 in ovariectomized diabetic rats. These results, taken together, suggest that chronic administration of 17β‐estradiol produced a protective effect in the systemic vasculature in streptozotocin‐induced diabetic rats. This is the first in vivo study showing this protective effect of 17β‐estradiol during diabetes.This project was financially supported by Conacyt (Grant number 152534).Grant Funding Source: Supported by Conacyt 152534