CONTRIBUTION OF ALPHA-ADRENOCEPTORS TO DEPOLARIZATION AND CONTRACTIONEVOKED BY CONTINUOUS ASYNCHRONOUS SYMPATHETIC-NERVE ACTIVITY IN RAT TAIL ARTERY

1 The effects of continuous but asynchronous nerve activity induced by ciguatoxin (CTX-1) on the membrane potential and contraction of smoot h muscle cells have been investigated in rat proximal tail arteries is olated in vitro. These effects have been compared with those produced by the continuous application of phenylephrine (PE). 2 CTX-I (0.4 nM) and PE (10 mu M) produced a maintained depolarization of the arterial smooth muscle that was almost completely blocked by alpha-adrenoceptor blockade. In both cases, the depolarization was more sensitive to the selective alpha(2)-adrenoceptor antagonist, idazoxan (0.1 mu M), than to the selective alpha(1)-adrenoceptor antagonist, prazosin (0.01 mu M) 3 In contrast, the maintained contraction of the tail artery induce d by CTX-1 (0.2 nM) and PE (2 and 10 mu M) was more sensitive to prazo sin (0.01) mu M, than to idazoxan (0.01 mu M). In combination, these a ntagonists almost completely inhibited contraction to both agents. 4 A pplication of the calcium channel antagonist, nifedipine (1 mu M), had no effect on the depolarization induced by either CTX-1 or PE but max imally reduced the force of the maintained contraction to both agents by about 50%. 5 We conclude that the constriction of the tail artery i nduced by CTX-I, which mimics the natural discharge of postganglionic perivascular axons, is due almost entirely to alpha-adrenoceptor activ ation. The results indicate that neuronally released noradrenaline act ivates more than one alpha-adrenoceptor subtype. The depolarization is dependent primarily on alpha(2)-adrenoceptor activation whereas the c ontraction is dependent primarily on alpha(1)-adrenoceptor activation. The links between alpha-adrenoceptor activation and the voltage-depen dent and voltage-independent mechanisms that deliver Ca2+ to the contr actile apparatus appear to be complex.