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Plasma vasopressin (AVP) levels were measured at rest (mean arterial pressure 80–85 mmHg) and during hypotension (mean arterial pressure 38–45 mmHg) induced by ganglionic blockade (trimethaphan) in halothane-anaesthetized respirated rats with end-tidal pCO₂ maintained at 34–40 mmHg. Hypotension (15 min) produced a 310% increase in plasma AVP (±60% S.E.M.) which was not reduced significantly by prior baro- and chemoreceptor denervation. The hypotension-induced rise in AVP was blocked by bilateral microinjections (40 nl) of the GABA-mimetic agent muscimol (151 pmol) into the ventrolateral medulla at obex level and significantly attenuated by injections of the same amount in the nucleus tractus solitarius. The rise in AVP was unaffected by microinjections in the pontine locus coeruleus. It was also blocked by bilateral microinjections of the glutamate-receptor antagonist kynurenate (40 nl, 1·8 nmol) into the ventrolateral medulla but unaffected by microinjections of the inactive analogue xanthurenic acid (40 nl, 1·8 nmol). A significantly smaller rise in plasma AVP (88%) was observed following bilateral nephrectomy. It is concluded that, in this preparation, hypotension produces the release of AVP via a mechanism largely independent of baro- and chemoreceptors, which requires the activation of neurones located in the caudal medulla oblongata. The same or closely related neurones may be activated by a neural or hormonal signal generated by the kidney.

J. Endocr. (1988) 118, 101–111

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