Mechanisms of vasodilation induced by vasoactive intestinal polypeptide in rabbit mesenteric artery

Publisher Website
Google Scholar
Abstract
Vasoactive intestinal polypeptide (VIP; over 10-13 M) inhibited the norepinephrine (NE)-induced contraction evoked from the rabbit mesenteric artery. Increased concentrations of VIP (over 10-9 M) inhibited the contractions induced by caffeine and 39 mM [K]o. However, VIP (< 10-7 M) had no effect on the membrane potential and resistance of muscle cells. In Ca-free solution, VIP (10-10 M) inhibited the NE-induced contraction, but the 2nd application of NE after removal of VIP enlarged the amplitude of contraction over that in the control. Yet when 10-9 M VIP was applied, both the 1st and 2nd contractions were consistently smaller than those observed by application of 10-10 M VIP. In Na- and Ca-free solution, repetitive applications of NE generated contractions longer than those observed in Ca-free solution. When VIP (10-10 M) was applied once (3 min), the contraction was inhibited only once during repetitive applications of NE. VIP (over 10-9 M) dose dependently inhibited the NE-induced contraction and had a long-lasting inhibition after washout of the tissue. In saponin-treated skinned muscles, VIP (10-7 M) had no effect on the Ca-induced contraction or on the Ca store sites. VIP (> 10-8 M) was .apprx. 10 times more potent than equimolar concentrations of isoproterenol in increasing the content of cAMP. VIP (10-10 M) apparently selectively inhibits the Ca release activated by NE, and high concentrations (over 10-9 M) would expectedly increase the Ca extrusion from cells following increase in the levels of cAMP.