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Search for other papers by M. W. SMITH in
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Search for other papers by N. A. THORN in
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SUMMARY
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.
Search for other papers by T. E. BRIDGES in
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Search for other papers by N. A. THORN in
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SUMMARY
Intracarotid injection of 0·25 ml of a hyperosmotic (1 m) sodium chloride solution into hydrated rats was an effective stimulus for vasopressin release. The effects of autonomic blocking drugs on this stimulus and on the release of vasopressin by intracarotid injections of acetylcholine were studied.
Anti-adrenergic compounds (reserpine and phenoxybenzamine), ganglion-blocking agents (pempidine and pentolinium) and atropine were shown to be effective in preventing the vasopressin release caused by hyperosmotic stimulation.
Acetylcholine-induced release of vasopressin was inhibited by pempidine but not reserpine.
Based on these findings the nervous pathway(s) involved in the release of vasopressin induced by hyperosmolarity of the plasma is discussed.
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Search for other papers by E. SKADHAUGE in
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SUMMARY
Calcium chloride was infused intravenously as a slightly hypotonic solution into hydrated rats anaesthetized with ethanol and Inactin. Doses of 12–24 mg. Ca2+/kg. caused a transitory antidiuretic effect during which time antidiuretic material was excreted in the urine. Intracarotid infusion of calcium chloride towards the head produced a more pronounced effect than intravenous infusion of the same amount. The same doses of calcium chloride failed to have an antidiuretic effect in rats with diabetes insipidus.
These findings are discussed in relation to the hypothesis of Douglas & Poisner that calcium ions play an essential role in the release of vasopressin from the posterior pituitary gland.
