Vasopressin release from incubated in situ posterior pituitary lobe after intraventricular injection of carbachol or atropine.
The vasopressin release rate from incubated in situ rats posterior pituitary lobe as observed following intracarotid infusions of hypertonic solutions (3 x 0.1 ml/100 g b.w. contained 1.0 mmol NaCl and 0.1 mmol CaCl2 per 1 ml) was studied when influenced by intraventricular injections of 0.6 microgram carbachol or 240 microgram atropine sulphate, respectively. The increase in the release of vasopressin following intracarotid infusions of hypertonic solution augmented by intraventricular injection of carbachol was found. Atropine was shown to be effective in preventing the vasopressin release caused by hypertonic solution. The effects of carbachol and atropine indicate that mediation at synapses in the nucleus supraopticus involved in the release of vasopressin induced by osmotic stimulation is cholinergic.
D000818:Animals; D001285:Atropine / Q000494:pharmacology*; D002217:Carbachol / Q000494:pharmacology*; D007276:Injections, Intraventricular; D008297:Male; D010904:Pituitary Gland, Posterior / Q000187:drug effects / Q000378:metabolism*; D051381:Rats; D014667:Vasopressins / Q000378:metabolism*
D014667:Vasopressins; D001285:Atropine; D002217:Carbachol