Abstract
This study concerns the role of arginine-vasopressin (AVP) for the development of hypertension after constriction of the abdominal aorta proximal to the renal arteries (PAC). The PAC was applied in AVP-deficient Brattleboro (Bb) rats and the blood pressure was recorded 3 weeks later. In untreated rats, PAC did not cause hypertension. When the rats were given AVP 0.6 or 6 nmol day-1 for 2 weeks using mini-pumps, hypertension developed both proximal and distal to the constriction. The level of the hypertension was independent of the AVP dose. When the rats were given I-deamino-4-valine-8-D-arginine-vasopressin (dVDAVP) a specific antidiuretic agonist without effect on the vascular AVP receptors, hypertension did not develop. Sham-operated rats given AVP did not develop hypertension. The PAC rats treated with AVP but not with dVDAVP had an enhanced pressor response to an i.v. bolus dose of angiotensin II. It is concluded that AVP plays an important role in the development of hypertension following aortic constriction and that the action is mediated via the vascular AVP-receptors. We suggest that the presence of AVP permits the expression of other hypertensive factors, such as angiotensin II.
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