The Tohoku journal of experimental medicine
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Tohoku J. Exp. Med. · Jul 1976
Peripherally and centrally mediated bradycardiac effects of clonidine in anesthetized or spinal rats.
The bradycardia-inducing effects of clonidine were examined in anesthetized or spinal rats by injecting the drug intracisternally (i.c.) or intravenously (i.v.). Clonidine (1-25mug i.c.) caused a bradycardia dose-dependently in anesthetized rats. The bradycardia in response to clonidine (5mug i.c.) was significantly reduced after a treatment with phentolamine (100 mug i.c.), but not influenced with atropine (1 mg i.v.) or sectioning bilateral cervical vagal nerves. ⋯ This inhibition by clonidine was antagonized by phentolamine (5 mg i.v.). Clonidine (30 mug i.v.) did not significantly influence the acceleration in heart rate of spinal rats induced by norepinephrine (1 mug i.v.), tyramine (100 mug i.v.) or 1,1-dimethyl-4-phenylpiperazinium (DMPP, 50 mug i.v.). Therefore, it is suggested that clonidine causes a bradycardia by stimulating both peripheral and central alpha-adrenoceptors, the sympathetic trunk is the main pathway, and that the peripheral mechanism for clonidine-induced bradycardia is different from the action of guanethidine or hexamethonium on a release of catecholamines from the cardiac nerve terminals.