Hypercalcaemia produced in rats by the intravenous injection of calcium chloride, slowed the rate of disappearance of injected vasopressin from the blood circulation. 24% of the vasopressin injected appeared in the urine of hypercalcaemic rats compared with 7 % in control animals.
Vasopressin injected intravenously into control rats was distributed in a volume equal to the blood volume but when rats had been made hypercalcaemic, the theoretical volume of distribution was three to four times greater. Antidiuresis produced by injection of large doses of vasopressin into hydrated rats was little affected by changes in the blood concentration of calcium. Calcium chloride injected intravenously into hydrated rats resulted in a temporary antidiuresis.
Experiments in vitro with Sephadex G-25 showed that both ox neurophysin and rat serum protein bind vasopressin and that calcium interferes with the binding.
It is suggested that calcium can compete directly with vasopressin for acidic binding sites on proteins; that this can cause the release of vasopressin and alter the transport and possibly the rate of inactivation, of vasopressin.
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