alpha-Adrenoceptor mediated contractile and electrical responses of vascular smooth muscle.

Concentration-response curves for the contractile effects of noradrenaline and the alpha 1-adrenoceptor agonist methoxamine, obtained in strips of rabbit main pulmonary artery under various experimental conditions, characterized methoxamine as a full agonist with approximately one-third of the potency of noradrenaline. As measured with intracellular glass microelectrodes, both agonists depolarized the vascular smooth muscle cells over the lower segment of the concentration-contraction curve without further depolarization over the upper segment, indicating that part of the contraction occurred in the absence of changes in membrane potential. The similarity between noradrenaline and methoxamine with regard to induction of electrical events and contraction and the complete blockade of the two types of response by the alpha 1-antagonist prazosin suggest that the effects of both agonists are mediated in the rabbit main pulmonary artery mainly, if not exclusively, by alpha 1-adrenoceptors. In contrast to the induced changes in membrane potential, membrane resistance was decreased by methoxamine over the entire range of the concentration-contraction curve as determined by measurement of the space constant of the vascular strips. This points to the occurrence of alpha 1-adrenoceptor mediated changes of membrane properties which are not reflected by alterations in membrane potential. It is concluded that contraction induced in the rabbit main pulmonary artery by stimulation of alpha 1-adrenoceptors is better described by the term electromechanical than pharmacomechanical coupling.