Evidence that Nitric Oxide Can Act Centrally to Stimulate Vasopressin Release

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Abstract
Nitric oxide (NO) is the endothelium-derived relaxing factor, which causes relaxation of vascular smooth muscle. NO synthetase, the enzyme for the synthesis of NO from its precursor L-arginine, is also widely distributed in neurons in the brain, and it has been suggested that NO may serve as an important neuromodulator. Because NO synthetase is present in the hypothalamus in relatively high concentration, we have determined whether NO can affect the release of vasopressin in conscious, chronically prepared rats. The intra-cerebroventricular (i.c.v.) injection of S-nitroso-N-acetylpenicillamine (12.5 and 25 µg; SNAP), that spontaneously breaks down to form NO, caused transient dose-related increases in the plasma vasopressin concentration of 1 and 2 µU/ml (p

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