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SUMMARY
The uptake of 32P into the rat neural lobe and hypothalamus was studied after intraperitoneal and intraventricular (lateral ventricle of the brain) administration of the isotope. After intraventricular injection the uptake into both tissues was greater by up to three orders of magnitude than after intraperitoneal administration. Maximum uptake of isotope after intraventricular injection occurred at 4 h in the hypothalamus and at 48 h in the neural lobe. Incorporation of isotope into phospholipids was maximal at 24 h in both the hypothalamus and neural lobe.
Isolated neurosecretory granules and small vesicles contained 46·5 ± 2·3% and 11·9 ± 1·7% respectively of the total phospholipids found in particulate fractions of neural lobe homogenates. Two-dimensional thin-layer chromatography showed that all seven phospholipids tested for occurred in both the isolated neurosecretory granules and small vesicles.
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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.
