Calcium Stimulates Vasopressin Release

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The association of acute hypercalcaemia with hypertension has long been known. Its mechanism has remained unexplained, however, since no significant pressor contribution from the renin-angiotensin system or the sympathetic nervous system has been detected. To assess the possible contribution of arginine vasopressin (AVP), we investigated the effect of a 2 h infusion of 2 ml isotonic calcium gluconate (0.46 mmol/ml Ca2+) on the mean blood pressure of anephric (n=8) or intact (n=7) rats and the blood pressure response to a specific vasopressin inhibitor (V,). In anephric rats, blood pressure rose by 30 ± 3 mmHg (mean ± s.e.m.) and plasma AVP levels rose to 34 ± 9 pg/ml. In response to injection of the AVP inhibitor, blood pressure fell by 26 ± 3 mmHg. In intact rats, blood pressure rose by 12 ± 4 mmHg with plasma AVP levels 14.5 ± 3.2 pg/ml (normal range 2.2 ±1.1 pg/ml), but did not respond consistently to AVP inhibition. Serum calcium levels at the end of the infusion were 25.0 ± 4.3 mg/dl in anephric and 24.9 ± 1.2 mg/dl in intact rats. In order to confirm that the calcium ion was indeed responsible for the AVP-dependent changes in blood pressure, another group of anephric rats (n=8) received a 2 h infusion of CaCI2 (0.46 mmol/ml Ca2+) and exhibited a blood pressure rise of 35 ± 3 mmHg, which responded to the AVP inhibitor with a blood pressure fall of 22 ± 3 mmHg. Moreover, prior treatment with indomethacin greatly attenuated the pressor effect of calcium infusion and prevented the rise of AVP. We conclude that acute hypercalcaemia induces a pressor response and a stimulation of AVP release, both of which appear to be modulated by renal and extrarenal prostaglandins.

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