Role of vasopressin in cardiovascular response to central cholinergic stimulation in rats.

Abstract

The cardiovascular effects of centrally administered cholinomimetics were examined in conscious Long-Evans and Brattleboro rats. Carbachol (1 ^tg/kg) or physostigmine (50 /ug/kg) induced a long-lasting increase in blood pressure and a decrease in heart rate in Long-Evans rats whereas no bradycardia was observed in Brattleboro rats, and the pressor response was significantly less than that in Long-Evans rats. The cardiovascular responses to nicotine (30 jtg/ kg) in Brattleboro rats were not different from those in Long-Evans rats. Intravenous vasopressin antagonist, dfCH^jTyrCMe) arginine vasopressin, significantly attenuated the pressor response and eliminated the bradycardic response to carbachol hi Long-Evans rats. However, the pressor response to carbachol in Brattleboro rats was still significantly less than that in Long-Evans rats treated with vasopressin antagonist. Intravenous phentolamine partially inhibited the pressor response to carbachol in Long-Evans rats and completely eliminated it in Brattleboro rats. Combined intravenous treatment with phentolamine and vasopressin antagonist completely eliminated the pressor response to carbachol in Long-Evans rats. Centrally administered methylatropine eliminated either the hypertensive or bradycardic response to carbachol in Long-Evans rats. These results indicate that the pressor and bradycardic response to carbachol or physostigmine is mediated by the central muscarinic receptor mechanism. Hypertensive response to intracerebroventriculaiiy administered carbachol in normal rats is mediated both by an increase in central sympathetic outflow and in circulating vasopressin. The bradycardia seems to be mediated mainly by vasopressin. {Hypertension 1989;13:549-557)

The Association of Cardiovascular Responses with Brain c-fos Expression after Central Carbachol in the Near-Term Ovine Fetus

“…Moreover, the increased fetal systolic, diastolic, and MAP maintained at a high level for more than 90 min. Accompanied with the increase of BP, the fetal heart rate decreased, which was also similar to that of the adults (Imai et al, 1989). In the present study, the fetal heart rate decreased immediately after the i.c.v.…”

Hydrogen peroxide attenuates the dipsogenic, renal and pressor responses induced by cholinergic activation of the medial septal area

“…* Different from PBS (Two-away ANOVA, followed by Student-NewmanKeuls, p < 0.05). (Hoffman et al, 1977;Imai et al, 1989). Cholinergic activation of the MSA increased the activity of the vasopressinergic neurons in the PVN and the pre-treatment of the MSA with H 2 O 2 , similarly reduced MSA carbacholinduced pressor response and activation of vasopressinergic neurons in the mPVN, which suggests that reduction of vasopressin secretion is a possible reason for the reduced pressor response in rats pre-treated with H 2 O 2 in the MSA.…”

“…Increased activity of vasopressinergic and oxytocinergic cells in the PVN and/or SON and the release of the respective hormones is probably the mechanism activated by carbachol in the MSA to produce antidiuresis and natriuresis. Central cholinergic activation increases plasma AVP and part of the antidiuresis induced by central cholinergic stimulation, including that produced by MSA activation, is attributed to AVP secretion, whereas the natriuresis induced by central cholinergic stimulation is suggested to depend on direct renal effects of OT and also on OT action stimulating the secretion of ANP by the cardiac myocytes (Hoffman et al, 1977;Tanaka et al, 1988;Imai et al, 1989;Huang et al, 1995;Antunes-Rodrigues et al, 2004). The pre-treatment with H 2 O 2 in the MSA reduced c-Fos expression in the vasopressinergic and oxytocinergic cells in the magnocellular PVN and/or SON.…”

Cholinergic stimulation with pyridostigmine protects myocardial infarcted rats against ischemic-induced arrhythmias and preserves connexin43 protein

“…One hour after the administration of saline or PYR, rats were treated with the cardiac autonomic receptor blockers methylatropine (1 mg/kg iv) and propranolol (2 mg/kg iv) at intervals of 15 min to indirectly assess cardiac parasympathetic and sympathetic autonomic tonus. The doses of methyl-atropine and propranolol used in the present study are well accepted as effective blockers of cardiac muscarinic and ␤-adrenergic receptors in rats (17,23,56). Half of the rats in each group (saline or PYR) received the autonomic blockers in the opposite order, i.e., propranolol followed by methyl-atropine.…”