Decreased pressor responsiveness in pregnancy: studies in experimental animals.
Pregnant animals of several species are resistant to the pressor effects of vasoconstrictor substances. Although a blunted pressor response to angiotensin II (AII) has been most thoroughly documented, resistance to the pressor effects of norepinephrine (NE), and arginine vasopressin (AVP) has also been found. In this review, possible mechanisms for decreased pressor responsiveness are discussed. Although antagonism of vasoconstriction by vasodilatory prostaglandins is the most likely cause for decreased pressor responsiveness in pregnancy, other possibilities have been proposed. Reduced pressor responsiveness to AII occurs in many conditions other than pregnancy, and the mechanisms involved include down-regulation of AII receptors, increased production of vasodilatory prostaglandins (as in pregnancy), and post-receptor defects in AII action. Several recent studies have also suggested a role of the sex hormones, particularly 17-beta-estradiol and prolactin, in stimulating prostaglandin production and causing the decreased pressor response to AII in pregnancy.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001127:Arginine Vasopressin / Q000494:pharmacology; D001794:Blood Pressure / Q000187:drug effects; D005260:Female; D009638:Norepinephrine / Q000494:pharmacology; D011191:Potassium Deficiency / Q000503:physiopathology; D011247:Pregnancy; D011270:Pregnancy, Animal / Q000502:physiology*; D011453:Prostaglandins / Q000502:physiology; D012964:Sodium / Q000172:deficiency
D011453:Prostaglandins; D000804:Angiotensin II; D001127:Arginine Vasopressin; D012964:Sodium; D009638:Norepinephrine