HYPERTENSIVE RESPONSE TO ACUTE AORTIC COARCTATION IN CHRONIC VASOPRESSIN DEFICIENT STATES

We investigated the genesis of the hypertensive response to acute (45 min) aortic constriction in two models of chronic vasopressin (AVP) de ficiency, i.e., Brattleboro strain and median eminence lesioned (MEL) Wistar rats. The same degree of partial aortic constriction, with a pn eumatic cuff placed around the abdominal aorta, yielded a sudden and m aintained increase in carotid pressure to the same extent in Brattlebo ro, MEL and sham-MEL rats. Blockage of AVP V-1 receptors with d(CH2)(5 )Tyr[Me]AVP did not affect the hypertensive response of Brattleboro or MEL rats, but gradually blunted the response of sham-MEL rats. Blocka ge of angiotensin II receptors with saralasin blunted the hypertensive response of the AVP-deficient subjects throughout the experiment, but only delayed (5-15 min) the onset of hypertension in sham-MEL rats. S imultaneous blockage of AVP and angiotensin II blunted the hypertensiv e response of sham-MEL and AVP-deficient rats throughout the experimen t. These data demonstrate that when one vasoactive system is chronical ly absent, as is the case for AVP in Brattleboro and MEL rats, the ren in-angiotensin system plays the major role in the pathophysiology of a cute aortic coarctation hypertension.