To determine whether endogenous oestrogen plays a role in pregnancy induced decreased vascular reactivity we have examined the effects of 17 beta-oestradiol on vasoconstrictor responses to various stimuli using an in situ blood-perfused mesenteric vascular preparation in Wistar-Kyoto (WKY) rats. 2. Daily administration of 17 beta-oestradiol (500 micrograms/kg, s.c.) for 15 days significantly enhanced mesenteric vasoconstrictor responses to noradrenaline (NA), without affecting responses to the electrical stimulation of sympathetic nerves (ES) and angiotensin II (AngII). 3. Nitric oxide (NO) synthesis inhibition by nitro-L-arginine methyl ester (L-NAME; 100 mg/kg, i.v.) significantly potentiated mesenteric vasoconstrictor responses to all stimuli in both 17 beta-oestradiol-treated and control animals. The difference in NA responses between groups was diminished following NO synthesis inhibition. 4. These findings do not support the hypothesis that increased endogenous oestrogen plays a role in decreased mesenteric vascular reactivity in pregnancy. However, responses to oestrogen may be dose-dependent and enhancement of vasoconstrictor responses to NA may be relevant to oral contraceptive-induced hypertension.
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Chu et al. (1997) studied this question.
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