The role of activation of the renin–angiotensin system on the reflex regional vasoconstriction caused by distension of the uterus in anaesthetized pigs

Abstract

Distension of the uterus in anaesthetized pigs has been shown to cause a reflex regional vasoconstriction and an increase in plasma renin activity (PRA) through efferent sympathetic mechanisms which respectively involved α- and β-adrenergic receptors. The present study was undertaken to determine the possible contribution of the activation of the renin–angiotensin system (RAS) to the observed regional vasoconstrictive responses to uterus distension. In pigs anaesthetized with α-chloralose, blood flow in the left circumflex or anterior descending coronary, superior mesenteric, left renal and left external iliac arteries was assessed using electromagnetic flowmeters. Distension of the uterus for periods of 30 min was performed by injecting 20 ml of warm Ringer solution into balloons positioned within the viscus before and after blockade of angiotensin II receptors with losartan. Changes in heart rate and renal blood flows were respectively prevented by atrial pacing and injection of phentolamine into the renal arteries. Changes in baroreceptors activity and in regional perfusion pressure were minimized by section of cervical vagus nerves and denervation of carotid sinuses and by an aortic constriction. PRA was assessed during the last minute of distension by radioimmunoassay of angiotensin I. Before blockade of angiotensin II receptors, in six pigs, distension of the uterus decreased coronary blood flow by 19%, and in other six pigs, decreased mesenteric and iliac blood flows by 13.1% and 29.4% in the absence of changes in arterial perfusion pressure. After losartan, these decreases were significantly reduced to 11.7%, 8.2% and 18%. These results showed that the activation of the RAS significantly contributed to the α-adrenergic receptor-mediated regional vasoconstrictive responses reflexly elicited by distension of the uterus.