V. Savci et Ih. Ulus, CHOLINE ADMINISTRATION REVERSES HYPOTENSION IN SPINAL-CORD TRANSECTEDRATS - THE INVOLVEMENT OF VASOPRESSIN, Neurochemical research, 23(5), 1998, pp. 733-741
Intracerebroventricular (i.c.v.) choline (50-150 mu g) increased blood
pressure and decreased heart rate in spinal cord transected, hypotens
ive rats. Choline administered intraperitoneally (60 mg/kg), also, inc
reased blood pressure, but to a lesser extent. The presser response to
i.c.v. choline was associated with an increase in plasma vasopressin.
Mecamylamine pretreatment (50 mu g; i.c.v.) blocked the presser, brad
ycardic and vasopressin responses to choline (150 mu g). Atropine pret
reatment (10 mu g; i.c.v.) abolished the bradycardia but failed to alt
er presser and vasopressin responses. Hemicholinium-3 [HC-3 (20 mu g;
i.c.v.)] pretreatment attenuated both bradycardia and presser response
s to choline. The vasopressin V1 receptor antagonist, rcapto-beta,beta
-cyclopenta-methylenepropionyl(1), O-Me-Tyr(2), Arg(8))-vasopressin (1
0 mu g/kg) administered intravenously 5 min after choline abolished th
e presser response and attenuated the bradycardia-induced by choline.
These data show that choline restores hypotension effectively by activ
ating central nicotinic receptors via presynaptic mechanisms, in spina
l shock. Choline-induced bradycardia is mediated by central nicotinic
and muscarinic receptors. Increase in plasma vasopressin is involved i
n cardiovascular effects of choline.