EFFECT OF MEDIAN-EMINENCE LESION ON THE HYPERTENSIVE RESPONSE DUE TO ACUTE AORTIC COARCTATION

The present study was designed to investigate the effect of a lack of vasopressin resulting from electrolytic lesion of the median eminence of the hypothalamus on the acute 45-min aortic coarctation hypertensio n elicited in conscious rats by means of a pneumatic cuff placed aroun d the aorta above the renal arteries. Forty-eight hours after lesion, aortic constriction elicited a prompt (5-min) rise in mean carotid pre ssure from 115 +/- 2 to 149 +/- 2 mmHg, followed by a gradual decline to 129 +/- 2 mmHg. In contrast, sham-lesioned rats exhibited a prompt hypertensive response from 118 +/- 2 to 157 +/- 2 mmHg that leveled of f throughout the experiment. Lesioned rats treated with saralasin pres ented a blunted hypertensive response (within 125 +/- 2 to 130 +/- 2 m mHg), whereas sham-lesioned rats showed only a delay in the onset of h ypertension. The hypertensive response of lesioned rats was unaffected by the vasopressin antagonist [d(CH2)(5)Tyr(Me)]AVP, whereas sham-les ioned rats submitted to this treatment presented a prompt rise in pres sure followed by a gradual decline at the end of the experiment. Lesio ned and sham-lesioned rats treated with saralasin plus vasopressin ant agonist showed a blunted hypertensive response throughout the experime nt. These data demonstrate that the integrity of the median eminence p lays a pivotal role in the maintenance (30-45 min) of acute aortic coa rctation hypertension, presumably involving the release of vasopressin from the neurohypophysis, whereas angiotensin II mainly accounts for the prompt (5-15 min) rise in pressure.