Intracerebroventricular choline reverses hypotension induced by acute chemical sympathectomy

1: The effect of centrally administered choline on blood pressure was investigated in rats made hypotensive by chemical sympathectomy. Chemical sympathectomy was produced by intravenous (i.v.) injection of 50 mg kg(-1) of 6-hydroxydopamine (6-OHDA). Intracerebroventricular (i.c.v.) administration of choline (50-150 mu g) 2 h after 6-OHDA treatment increased blood pressure and reversed the hypotension in a dose-dependent mariner without affecting heart rate. The presser response was associated with an increase in plasma vasopressin levels. 2: Pretreatment of rats with the nicotinic receptor antagonist, mecamylamine (50 mu g, i.c.v.), but not the muscarinic receptor antagonist atropine (10 mu g, i.c.v.), blocked both the presser and vasopressin responses to choline (150 mu g). Pretreatment of rats with hemicholinium-3 (HC-3), a high affinity choline uptake inhibitor, greatly attenuated the presser response to i.c.v. choline (150 mu g). 3: The vasopressin V1 receptor antagonist, (beta-mercapto-beta,beta-cyclopentamethylenepropionyl-O- Me-Try,Arg)-vasopressin (10 mu g kg(-1); i.v.), given 5 min after i.c.v. choline, decreased the blood pressure but failed to return it to the pre-choline levels. Prazosine (0.5 mg kg(-1); i.p.), an antagonist of a-adrenoceptors, also decreased blood pressure. Administration of both antagonists together eliminated the presser response to choline, and the blood pressure was reduced further to below the pre-choline levels. 4: It is concluded that i.c.v. choline can increase blood pressure in rats made hypotensive by acute chemical sympathectomy through the activation of central nicotinic receptors by presynaptic mechanisms. An elevation in plasma levels of both vasopressin and catecholamines (possibly released from the adrenal medulla) is involved in the pressor response to choline