Termination of digitalis‐induced ventricular tachycardias by clonidine involves central α 2 ‐adrenoceptors in cats

1 Effects of intravenous (i.v.) and intravertebral arterial (i.a.) administration of the α 2 ‐adrenoceptor agonist, clonidine (Clon) and its antagonist, yohimbine (Yoh, 0.5 mg kg −1 , i.v.; 0.05 mg kg −1 , i.a.), on ventricular tachycardia (VT) induced by intravenous acetylstrophanthidin (AS) were studied in cats anaesthetized with intraperitoneal chloralose. 2 AS dose‐dependently produced cardiac arrhythmias including complete atrioventricular conduction block (118 ± 14 μg kg −1 , i.v.), junctional tachycardia (128 ± 20 μg kg −1 , i.v.), multiform ventricular premature beats (157 ± 21 μg kg −1 , i.v.) and sustained VT (220 ± 23 μg kg −1 , i.v.). 3 Doses of Clon (i.v.) required for termination of VT following i.v. Yoh (62.9 ± 5.2 μg kg −1 ) or i.a. Yoh (88.5 ± 16.3 μg kg −1 ) were higher than those for termination of VT without Yoh administration (28.3 ± 6.2 μg kg −1 ). Doses of Clon (i.a.) required for termination of VT without or with i.a. Yoh administration were 5.8 ± 1.0 or 14.8 ± 3.7 μg kg −1 , respectively, and they were significantly different. 4 These experiments demonstrate that either i.v. or i.a. Yoh antagonizes the antiarrhythmic effect of Clon on AS‐induced VT. Since small doses of Clon administered i.a. act predominantly on the central nervous system, we suggest that its antiarrhythmic effect is likely to be on central α 2 ‐adrenoceptors in the central nervous system.