VIP inhibition of vascular smooth muscle: complementary to beta 2-adrenoceptor mediated relaxation in the isolated rat portal vein.

Exogenous VIP caused a concentration dependent inhibition of the spontaneous mechanical activity in the isolated rat mesenteric-portal vein preparation via a mechanism which was completely independent of the propranolol-blocked beta-adrenoceptor, of high K+ in the medium and of exogenous bovine pancreatic polypeptide, neurotensin and opioids. The potency of VIP (pD2 = 7.52 +/- 0.18, n = 6) was about 30 times higher than that of isoprenaline in the atropine and phentolamine-blocked preparation. The isoprenaline inhibition was mediated via a beta 2-type of adrenoceptor with low apparent affinity for noradrenaline (intrinsic activity (alpha) = 0.27 +/- 0.01, n = 8). Opposite effects of exogenous VIP and noradrenaline were on the other hand observed in the atropinized and beta-blocked preparation. These results suggest that in the rat portal vein neuronal VIP and circulating adrenaline may be complementary in their antagonism of the alpha-adrenoceptor mediated increase in contractility.