Contribution of Vasopressin to the maintenance of blood pressure in deoxycorticosterone-salt induced malignant hypertension in spontaneously hypertensive rats

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Abstract
1. In the present study, deoxycorticosterone (DOC) and salt was administered to Wistar-Kyoto (WKY) rats and spontaneously hypertensive rats (SHR) by using silicone-rubber implants (DOC acetate, 100 mg/kg) and 0.9% NaCl as drinking water. SHR treated with DOC-salt for 4 weeks showed the characteristics of malignant hypertension including marked increase in blood pressure and left ventricular weight with typical histological changes in the kidney. 2. DOC-salt treatment increased plasma vasopressin levels in WKY (from 6.1 .+-. 0.5 to 8.9 .+-. 0.8 pmol/l) but significantly more in SHR (from 5.0 .+-. 0.6 to 15.8 .+-. 1.2 pmol/l). 3. Intravenous administration of the specific antagonist to the pressor effect of vasopressin, d(CH2)5Tyr(Me)AVP (10 .mu.g/kg), decreased mean arterial pressure of DOC-salt treated WKY and SHR by 6.6 .+-. 0.9 mmHg (P < 0.05) and 9.7 .+-. 1.7 mmHg (P < 0.05) respectively. 4. DOC-water treatment also increased plasma AVP levels in SHR to 10.5 .+-. 0.8 pmol/l, but the vasopressin antagonist had little effect on blood pressure in these rats. 5. Plasma levels of vasopressin were significantly correlated with both mean arterial pressure (r = 0.64) and left ventricular weight (r = 0.74). This suggest a close relationship between plasma AVP and severity of hypertension. 6. The results of the present experiment demonstrate that vasopressin is part of the overall pressor mechanism which contributes to the maintenance of blood pressure in DOC-salt induced malignant hypertension in SHR, but the small fall in pressure produced by the AVP antagonists suggests that the contribution is of only minor importance.

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