The role of brain angiotensin in thirst and AVP release induced by hemorrhage

Abstract

This study investigated the role of brain angiotensin (Ang II) in thirst induced by hemorrhage. Hemorrhage by blood withdrawal from the femoral artery to 33% and 44% blood volume loss produces a dose response increase in plasma Ang II. In the brainstem there was no Ang II response to hemorrhage. In the hypothalamus, Brain Ang II was maximally elevated to 33% hemorrhage. Thus, plasma Ang II and brain Ang II had an independent response to hemorrhage. To further test the role of central versus peripheral Ang II, we tested the effect of central (50 mg) and peripheral (50 mg/kg) administration of captopril or central injection of 1 mg losartan or 3 mg CGP 42112A prior to a 33% hemorrhage in unanesthetized male Sprague-Dawley rats (250 g). Drinking was measured and AVP blood samples were taken before and after hemorrhage. The results show that central (ivt) administration of captopril and losartan inhibited drinking compared to controls (0.33 ± 0.3 ml vs. 2.3 ± 0.8 ml: P < 0.05 and 0.20 ± 0.09 ml vs. 3.05 ± 0.81 ml; P < 0.01, respectively) while peripheral (ip) captopril alone increased drinking in response to hemorrhage (5.81 ± 0.81 ml vs. 2.3 ± 0.8 ml; P < 0.05). AVP levels were elevated at 5 and 15 min, but neither injections of losartan or CGP 42112A i.v.t. affected this response to hemorrhage. We conclude that increased hypothalamic brain Ang II after hypovolemic hemorrhage stimulates thirst and blood pressure restoration and acts through AT 1 receptors. The release of AVP in hemorrhage, however, does not rely exclusively on the angiotensinergic pathway in the brain.