Normal human pregnancy is characterized by vascular refractoriness to angiotensin II. This pregnancy-induced vascular refractoriness appears to be mediated principally by decreased vascular smooth muscle responsiveness to angiotensin II rather than by alterations in blood volume or plasma concentrations of renin or angiotensin II. The mechanism that controls vascular refractoriness during normal pregnancy likely involves a localized prostaglandin or prostaglandin-like action mediated through cyclic nucleotides. The action of progesterone or one of its metabolites appears to mediate the synthesis or the catabolism of locally produced prostaglandins or prostaglandin-like agents.
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