THE ROLE OF BRAIN ANGIOTENSIN IN THIRST AND AVP RELEASE INDUCED BY HEMORRHAGE

This study investigated the role of brain angiotensin (Ang II) in thir st induced by hemorrhage. Hemorrhage by blood withdrawal from the femo ral artery to 33% and 44% blood volume loss produces a dose response i ncrease in plasma Ang II. In the brainstem there was no Ang II respons e to hemorrhage. In the hypothalamus, Brain Ang II was maximally eleva ted to 33% hemorrhage. Thus, plasma Ang II and brain Ang II had an ind ependent response to hemorrhage. To further test the role of central v ersus peripheral Ang II, we tested the effect of central (50 mg) and p eripheral (50 mg/kg) administration of captopril or central injection of 1 mg losartan or 3 mg CGP 42112A prior to a 33% hemorrhage in unane sthetized 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 inhib ited drinking compared to controls (0.33 +/- 0.3 mi vs. 2.3 +/- 0.8 mi : P < 0.05 and 0.20 +/- 0.09 mi vs. 3.05 +/- 0.81 ml; P < 0.01, respec tively) while peripheral tip) captopril alone increased drinking in re sponse 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 lo sartan or CGP 42112A i.v.t. affected this response to hemorrhage. We c onclude that increased hypothalamic brain Ang II after hypovolemic hem orrhage stimulates thirst and blood pressure restoration and acts thro ugh AT, receptors. The release of AVP in hemorrhage, however, does not rely exclusively on the angiotensinergic pathway in the brain.