Two mechanisms underlie the slow noradrenergic depolarization in the rat tail artery in vitro

Abstract

In rat tail artery, short trains of electrical stimuli evoke both ATP-mediated excitatory junction potentials (EJPs) and a slow noradrenaline (NA)-mediated depolarization (NAD). Here we have investigated the contribution of α1- and α2-adrenoceptors to the NAD. The α1-adrenoceptor antagonist, prazosin (0.1μM), and the α2-antagonist, rauwolscine (1μM), reduced the amplitude of the NAD and in combination these agents virtually abolished the NAD. The KATP channel blocker, glibenclamide (10μM) abolished the α2-adrenoceptor-mediated component of the NAD, indicating that activation of these receptors produces closure of KATP channels. The α1-adrenoceptor-mediated component of the NAD was increased ..