A cholinergic link in the reflex release of vasopressin by hypotension in the rat.

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Abstract
Inhalation of amyl nitrite in the water-loaded rat under ethanol anesthesia produced a brief fall of blood pressure followed by a prolonged antidiuretic response. The antidiuretic response to amyl nitrite was accompanied by increased urinary excretion of vasopressin, it was blocked by a specific vasopressin antagonist and by a barbiturate and it was absent in the Brattleboro rat with congenital diabetes insipidus. The antidiuretic response to the hypotension induced by amyl nitrate apparently is due to the release of vasopressin and this release is mediated by a neuroendocrine reflex acting through the brain stem. Carbachol and nicotine produced an antidiuretic response on injection into a lateral cerebral ventricle (i.vent.). Carbachol was almost ineffective, but nicotine much more effective, when injected into the cisterna magna (i.cist.) from which in the rat there is no access to the ventricles. Carbachol therefore acts at a site reached from the ventricles, possibly the paraventricular nucleus. Nicotine acts at a more distal site reached from the subarachnoid space. This site may correspond with the nicotine-sensitive area on the ventral surface of the brain stem which was described in the cat. Atropine blocked the antidiuretic response to carbachol but not that to amyl nitrite. Hexamethonium blocked the antidiuretic response to amyl nitrate as well as that to nicotine and was more effective in i.cist. than i.vent. injection. These results reveal a cholinergic link with an nicotinic but not a muscarinic receptor in the neural pathways controlling the release of vasopressin in response to hypotension. A hypothetical model is presented in which the release of vasopressin is stimulated by a pathway arising from chemoreceptors and inhibited by a 2nd pathway arising from stretch- and baroreceptors. Hypotension acts by suppressing the normally predominant inhibitory pathway and stimulating the excitatory pathway. Hexamethonium is presumed to block transmission at a synapse in the excitatory pathway at the ventral surface or, less probably, at the paraventricular and supraoptic nuclei.