Role of the anteroventral third ventricle region and the renin angiotensin system in methylprednisolone hypertension

Abstract

Methylprednisolone (M, 10 mg/kg/week subcutaneously) was administered to cause hypertension in rats, and the role of AV3V region was assessed before and after development of the hypertensive state. Participation of the renin angiotensin system (RAS) was evaluated by changes in mean arterial pressure (MAP) induced by administration of saralasin (S, 10 μg/kg/min i.v.) or captopril (C, 20 mg/kg/p.o). An AV3V lesion before M administration partially prevented and delayed the beginning appearance of M hypertension. Furthermore, a prior AV3V lesion abolished an angiotensin II (AII)-dependent pressor component normally identified by S and C administration in this type of hypertension. During the maintenance phase of the hypertension, an AV3V lesion caused a partial reduction in blood pressure. A spontaneous disappearance of a vasoconstrictor component mediated by AH was observed in the late phases of M hypertension. It is concluded that the AV3V region is essential to the full development and maintenance of M hypertension in the rat. Also in this model, integrity of the AV3V area is essential to the expression of the All-mediated pressor component. Finally it is apparent that M can cause hypertension even in the absence of the A V3V area or during chronic renin angiotensin blockade, indicating multiple pathogenetic mechanisms in this experimental model. © 1981 American Heart Association, Inc.