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 alpha(2)-adrenergic and/or H-2-histaminerpic receptors, but not via activation of I-1-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 mu g/kg i.v.) elicited a decrease in mean arterial pressure (MAP) and heart rate (HR) dose-dependently. The dose of 10 mu g/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 alpha(2)-adrenoceptor and 5-HT1A receptor antagonist, blocked the cardiovascular responses to a subsequent i.v. injection of 10 mu g/kg clonidine. However, i.v. or i.c.v. preadministration of cimetidine, the H-2-histamine receptor antagonist, failed to antagonize the decreases in MAP and HR to a subsequent i.v. injection of IO mu g/kg clonidine. In addition, i.c.v. or i.v. pretreatment with the I-L-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 alpha(2)-adrenoceptor and/or 5-MT1A receptors and not through H-2-histamine or I-1-imidazoline receptors. (C) 1998 Elsevier Science B.V. All rights reserved.