|| Checking for direct PDF access through Ovid
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.