AJP - Heart and Circulatory Physiology, Vol 249, Issue 2 231-H240, Copyright © 1985 by American Physiological Society

ARTICLES

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

T. Itoh, T. Sasaguri, Y. Makita, Y. Kanmura and H. Kuriyama

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 (below 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 second 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 first and second 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 (over 10(-8) M) was about 10 times more potent than equimolar concentrations of isoproterenol in increasing the content of adenosine 3', 5'-cyclic monophosphate (cAMP). These results indicate that VIP (10(-10) M) 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.

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