Cardiovascular effects of intravenous administration of clonidine in conscious cats.

We previously reported that cardiovascular effects elicited by intracerebroventricular (i.c.v.) administration of clonidine result from stimulation of central alpha2-adrenergic and/or H2-histaminergic receptors, but not via activation of I1-imidazoline receptors in conscious cats. In this study, we investigated the effects on arterial blood pressure (MAP) and heart rate (HR) following an intravenous (i.v.) administration of clonidine using conscious cats. Injection of clonidine (2-10 microgram/kg i.v.) elicited a decrease in mean arterial pressure (MAP) and heart rate (HR) dose-dependently. The dose of 10 microgram/kg of clonidine decreased MAP and HR by 30+/-4 mmHg and 62+/-15 bpm, respectively. Intravenous or i.c.v. pretreatment with yohimbine, the alpha2-adrenoceptor and 5-HT1A receptor antagonist, blocked the cardiovascular responses to a subsequent i.v. injection of 10 microgram/kg clonidine. However, i.v. or i.c.v. preadministration of cimetidine, the H2-histamine receptor antagonist, failed to antagonize the decreases in MAP and HR to a subsequent i.v. injection of 10 microgram/kg clonidine. In addition, i.c.v. or i.v. pretreatment with the I1-imidazoline receptor blocker, efaroxan, failed to inhibit the cardiovascular effects of an i.v. administration of clonidine. These results demonstrate that i.v. clonidine evokes decreases in MAP and HR possibly via central alpha2-adrenoceptor and/or 5-HT1A receptors and not through H2-histamine or I1-imidazoline receptors.