The role of nitric oxide in the altered vascular reactivity of pregnancy in the rat

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Abstract
Pregnancy is characterized by a decrease in systemic vascular resistance and a blunting of the angiotensin II (AII) pressor response. We studied the role of nitric oxide (NO) and prostanoids in these vascular changes of pregnancy in anaesthesized, ganglion blocked non‐pregnant and pregnant rats. Inhibition of NO synthesis with NG‐nitro‐l‐arginine methyl ester (l‐NAME) led to an increase in mean arterial pressure (MAP) which was of a significantly greater magnitude in pregnant rats in late gestation than in non‐pregnant rats, or rats in mid‐gestation. The pressor response to varying doses of AII was attenuated during late pregnancy, and this attenuation was partially reversed by l‐NAME. The pressor response to varying doses of a vasocontrictor, phenylephrine (PE), was also attenuated in late pregnancy. However, this attenuation was not reversed by l‐NAME. Inhibition of prostanoid biosynthesis with meclofenamate did not alter basal MAP, nor the pressor response to varying doses of AII or PE in pregnant and non‐pregnant animals. It is concluded that (a) increased NO synthesis occurs during late gestation and contributes both to the decrease in systemic vascular resistance, as well as the blunting of the pressor response to AII during pregnancy, and (b) prostaglandins are not important in the maintenance of basal vascular tone, or the blunting of the pressor response to AII during pregnancy.

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