Cardiovascular effects of clonidine in an avian species, Larus argentatus

Blood pressure and heart rate were recorded in the sea gull, Larus argentatus, under light pentibarbitone anaesthesia. Clonidine 10(-7) and 10(-8) mol . kg-1 (27 and 2.7 microgram . kg-1) i.v. produced a biphasic effect on blood pressure, a brief initial increase being followed by a prolonged hypotensive response. There was an immediate reduction in heart rate rate which persisted throughout the hypotensive phase. After spinal transection at the level of C4, clonidine administration elicited hypertension and bradycardia. Bilateral vagotomy abolished the effect of clonidine on heart rate but did not alter the blood pressure response. Vagotomy in combination with spinal transection abolished the effect of clonidine on heart rate but the hypertensive response was accentuated. Yohimbine 10(-7) or 10(-6) mol . kg-1 (0.039 or 0.39 mg . kg-1) given 5 min after clonidine 10(-7) mol.kg-1 (27 microgram . kg-1) effectively antagonized the cardiovascular effects of clonidine, while prazosin 10(-7) or 10(-6) mol . kg (0.042 or 0.42 mg . kg-1) had no such effect. We conclude that clonidine acts in the central nervous system of the sea gull to produce a lowering of blood pressure and heart rate. These effects are mediated by central inhibition of sympathetic activity and, in the case of the heart rate, mostly by central activation of vagal activity to the heart. This central action of clonidine involves activation of alpha-adrenoceptors which are blocked by yohimbine but not by prazosin and therefore may belong to the alpha 2 subtype.