α2-adrenoceptors in rat resistance vessels

In pithed rats increases in blood pressure were induced by i.v. injections of the α1-agonist methoxamine and the α2-agonists clonidine, oxymetazoline and B-HT 920. The pressor responses were further analyzed by repeated measurements of cardiac output with the thermodilution technique and by calculation of total peripheral vascular resistance. During the pressor phase both vascular resistance and cardiac output were found to be elevated. This indicates that increases in both haemodynamic variables contributed to the pressure rise. Under the assumption that elevated vascular resistance reflected constriction of arterioles and elevated cardiac output constriction of capacitance vessels via increased venous return to the heart, and considering that the magnitude of the increase of both haemodynamic parameters was similar for all three agonists, the results suggest the existence of both α1- and α2-adrenoceptors in resistance as well as in capaticance vessels of rats. For α2-adrenoceptors in resistance vessels this conclusion was supported by the finding that the calcium antagonists verapamil and/or tiapamil virtually abolished the increases of blood pressure and vascular resistance in response to clonidine, oxymetazoline or B-HT 920, but not to methoxamine. The calcium antagonists did not affect the increases in cardiac output, irrespective of which type of α-agonist was administered. While the present results support the existence of α2-adrenoceptors in resistance vessels of the rat, they do not allow a firm conclusion as to their occurrence in rat capacitance vessels.