Cardiovascular effects of central administration of clonidine in conscious cats |
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Authors: | Ahmmed Ally |
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Affiliation: | aDepartment of Internal Medicine and Harry S. Moss Heart Center, UT Southwestern Medical Center, Dallas, TX 75235-9034, USA;bDepartment of Pharmacology and Biochemistry, University of New England, College of Osteopathic Medicine, 11 Hills Beach Road, Biddeford, ME 04005, USA |
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Abstract: | The effects on arterial blood pressure and heart rate after an intracerebroventricular (i.c.v.) administration of clonidine were investigated using conscious normotensive cats. Injection of clonidine (5–10 μg; 5 μl; i.c.v.) elicited a decrease in mean arterial pressure (MAP) and heart rate (HR) in a dose-dependent manner. The highest dose of 10 μg of clonidine decreased MAP and HR by 39 ± 3 mmHg and 74 ± 5 b.p.m., respectively (n = 7). Pretreatment with yohimbine, the α2-adrenoceptor antagonist (8 μg; 5 μl; i.c.v.) blocked the cardiovascular responses to a subsequent i.c.v. injection of 10 μg clonidine (n = 7). Furthermore, preadministration of cimetidine (100 μg; 5 μl; i.c.v.), the H2 histamine receptor antagonist with imidazoline receptor activating properties, prevented the decreases in MAP and HR to a subsequent i.c.v. injection of 10 μg clonidine (n = 7). By contrast, pretreatment with the specific I1 imidazoline receptor blocker, efaroxan (100–500 μg; 5 μl; i.c.v.), failed to inhibit the cardiovascular effects of an i.c.v. administration of 10 μg clonidine (n = 7). These results suggest that the effects of centrally administered clonidine on MAP and HR are probably not mediated through activation of the I1 subtype of imidazoline receptors in conscious cats. However, the cardiovascular effects elicited by i.c.v. administration of clonidine appear to result from stimulation of central α2-adrenergic or the H2 histaminergic-like receptors. |
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Keywords: | Arterial blood pressure α 2-Adrenoceptor Imidazoline receptor H2 histamine-like receptor Ventrolateral medulla Intracerebroventricular Heart rate |
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