Arginine vasopressin (AVP) has been found to contribute to the maintenance of blood pressure (BP) in the rat. Since potassium deficiency results in alterations in systemic hemodynamics, the role of AVP in the control of BP was studied after 14 to 21 days of dietary potassium deficiency. When potassium deficient and control rats were allowed free access to water, plamsa osmolality (301.4 ± 1 vs. 293.4 ± 3 mOsm/kg; P < 0.02) and plasma AVP (3.5 ± 0.2 vs. 2.4 ± 0.2 pg/ml; P < 0.02) were increased in potassium deficient animals. To determine the role of this increase in AVP in the maintenance of BP, BP was determined in rats made polydipsic by adding glucose to the drinking water. In both control and potassium deficient rats, increased fluid intake resulted in increased urine output, decreased urinary and plasma osmolality, and a decrease in plasma AVP. While there was no change in BP in control rats when fluid intake was increased, BP fell from 103.9 ± 1.8 to 96 ± 2.6 mmHg (P < 0.05) in potassium deficient rats with increased fluid intake. To confirm that the decrease in plasma AVP caused the decrease in BP in potassium deficient rats, an AVP pressor antagonist was employed. Following the administration of the AVP pressor antagonist, there was no change in BP in control animals. In contrast, BP fell from 104.3 ± 1.9 to 98.3 ± 2.5 mm Hg; P < 0.05 in potassium deficient rats. In addition, vasopressin infusion in potassium deficient rats with suppressed endogenous plasma AVP resulted in the restoration of BP to that observed in potassium deficient rats with an intact vasopressin system. In summary, potassium deficiency results in elevation in plasma AVP as a consequence of hyperosmolality. Since maneuvers which decreased either the content of action of AVP resulted in a decrease in BP in potassium deficient rats and since vasopressin infusion resulted in restoration of MAP in potassium deficient rats with suppressed endogenous plasma AVP, we conclude that AVP is important in the support of BP in the potassium deficient conscious rat.
Bibliographical noteFunding Information:
Portions of this work were presented in abstract form at the meeting of the Western Section, American Federation for Clinical Research in Carmel, California in February, 1982. This research was supported by National Institutes of Health grants AM 261056 and AM 07135. Dr. M. Manning generously supplied the AVP pressor antagonist. Dr. R. W. Schrier gave helpful advice in the course of these studies. P. Arnold and R. Marzic-Calvert provided expert technical assistance and C. Bignall provided secretarial assistance.