vasopressin--1-(1-mercaptocyclohexaneacetic-acid)-2-(o--methyl-l-tyrosine)-8-l-arginine- and Chronic-Disease

We investigated the genesis of the hypertensive response to acute (45 min) aortic constriction in two models of chronic vasopressin (AVP) deficiency, i.e., Brattleboro strain and median eminence lesioned (MEL) Wistar rats. The same degree of partial aortic constriction, with a pneumatic cuff placed around the abdominal aorta, yielded a sudden and maintained increase in carotid pressure to the same extent in Brattleboro, MEL and sham-MEL rats. Blockage of AVP V1 receptors with d(CH2)5Tyr[Me]AVP did not affect the hypertensive response of Brattleboro or MEL rats, but gradually blunted the response of sham-MEL rats. Blockage 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. Simultaneous blockage of AVP and angiotensin II blunted the hypertensive response of sham-MEL and AVP-deficient rats throughout the experiment. These data demonstrate that when one vasoactive system is chronically absent, as is the case for AVP in Brattleboro and MEL rats, the renin-angiotensin system plays the major role in the pathophysiology of acute aortic coarctation hypertension.

Topics: Angiotensin Receptor Antagonists; Animals; Antidiuretic Hormone Receptor Antagonists; Aortic Coarctation; Arginine Vasopressin; Blood Pressure; Chronic Disease; Female; Hormone Antagonists; Hypertension; Male; Median Eminence; Rats; Rats, Brattleboro; Rats, Wistar; Renin-Angiotensin System; Saralasin

The contribution of the paraventricular nucleus region of the hypothalamus (PVN) to the maintenance of one-kidney, figure-8 renal wrap hypertension was determined in this study. Electrolytic ablation of the PVN was performed 4 wk after the production of hypertension or sham operation. Ablation of the PVN region significantly reduced mean arterial pressure (MAP) from 150 +/- 9 to 110 +/- 3 mmHg in the hypertensive rats. In the sham-hypertensive group, the lesion decreased MAP from 118 +/- 2 to 99 +/- 4 mmHg. In both groups of animals MAP from 118 +/- 2 to 99 +/- 4 mmHg. In both groups of animals MAP returned to prelesion values by day 7 postlesion. When ganglionic blockade was performed on day 7 postlesion, the fall in MAP was greater in hypertensive rats (-44 +/- 5 mmHg) than in normotensive rats (-26 +/- 3 mmHg). In a separate group of rats studied 3 days after PVN ablation, ganglionic blockade produced similar decreases in MAP in the wrapped and sham-operated animals. These studies suggest that the PVN contributes to the increased functional sympathetic nervous system associated with one-kidney, figure-8 renal hypertension. Although ablation of the PVN region decreases MAP, neural mechanisms compensate to return MAP to hypertensive levels.

Topics: Animals; Arginine Vasopressin; Blood Pressure; Captopril; Chronic Disease; Heart Rate; Hypertension, Renal; Male; Paraventricular Hypothalamic Nucleus; Potassium; Rats; Rats, Inbred Strains; Reference Values; Sodium; Sympathetic Nervous System