Hypertension, Vol 13, 549-557, Copyright © 1989 by American Heart Association
Y Imai, K Abe, S Sasaki, N Minami, M Munakata, S Yumita, T Nobunaga, H Sekino and K Yoshinaga
The cardiovascular effects of centrally administered cholinomimetics were
examined in conscious Long-Evans and Brattleboro rats. Carbachol (1
microgram/kg) or physostigmine (50 micrograms/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 micrograms/kg) in Brattleboro rats
were not different from those in Long-Evans rats. Intravenous vasopressin
antagonist, d(CH2)5Tyr(Me) arginine vasopressin, significantly attenuated
the pressor response and eliminated the bradycardic response to carbachol
in 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 intracerebroventricularly 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.
ARTICLES
Role of vasopressin in cardiovascular response to central cholinergic stimulation in rats
Department of Medicine, Tohoku University School of Medicine, Sendai, Japan.
This article has been cited by other articles:
![]() |
L. Shi, C. Mao, F. Zeng, L. Zhu, and Z. Xu Central cholinergic mechanisms mediate swallowing, renal excretion, and c-fos expression in the ovine fetus near term Am J Physiol Regulatory Integrative Comp Physiol, February 1, 2009; 296(2): R318 - R325. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. V. Menani, S. P. Barbosa, L. A. De Luca Jr., J. I. F. De Gobbi, and A. K. Johnson Serotonergic mechanisms of the lateral parabrachial nucleus and cholinergic-induced sodium appetite Am J Physiol Regulatory Integrative Comp Physiol, March 1, 2002; 282(3): R837 - R841. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. H. Eckel Obesity and Heart Disease : A Statement for Healthcare Professionals From the Nutrition Committee, American Heart Association Circulation, November 4, 1997; 96(9): 3248 - 3250. [Full Text] |
||||
|
Hypertension Home | Subscriptions | Archives | Feedback | Authors | Help | AHA Journals Home | Search Copyright © 1989 American Heart Association, Inc. All rights reserved. Unauthorized use prohibited. |