Evidence of angiotensin II involvement in prolactin secretion in response to hemorrhage in adrenodemedullated and guanethidine-treated rats

Objective: The present experiments were designed to investigate the influence of the renin-angiotensin system (RAS) on prolactin secretion in response to hemorrhage (1.2ml/100g body weight (bw)/2min). Methods and Results: Male Wistar rats (250-300g) were divided into the following experimental groups. (i) Sham-operated animals submitted to intravenous administration of [Sar(1),Thr(8)]-angiotensin 11 (sarthran), an angiotensin 11 antagonist (750ng/100g bw as a bolus plus an infusion of 25ng/100g bw/min over 30min), which did not alter the prolactin secretion in response to hemorrhage. (ii) Animals submitted to adrenodemedullation which by itself increased the prolactin secretion in response to hemorrhage by 274% (P < 0.01). However, sarthran infusion into adrenodemedullated rats completely blocked this increased prolactin secretion in response to hemorrhage (P < 0.01). (iii) Intact animals submitted to blockade of sympathetic noradrenergic pathways by pretreatment with guanethidine (10mg/100g bw), which also increased the prolactin secretion in response to hemorrhage by 55% (P < 0.01). This increased prolactin secretion in response to hemorrhage observed in guanethidine-treated rats was completely blocked by sarthran preinfusion (P < 0.01). (iv) Adrenodemedullated animals pretreated with guanethidine, which abolished the prolactin secretion induced by hemorrhage. Conclusions: Our data suggest a role for circulating catecholamines in the prolactin secretion response to stress. In addition, the experiments reported here demonstrate that RAS has a stimulatory effect on prolactin secretion in circumstances in which sympathetic activity or adrenomedullary secretion is suppressed. These are the first data demonstrating that a physiological prolactin secretion response to stress depends on the RAS.