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 (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.
| Original language | English |
|---|---|
| Journal | American Journal of Physiology - Heart and Circulatory Physiology |
| Volume | 18 |
| Issue number | 2 |
| Publication status | Published - Jan 1 1985 |
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All Science Journal Classification (ASJC) codes
- Physiology
- Cardiology and Cardiovascular Medicine
- Physiology (medical)
Cite this
Mechanisms of vasodilation induced by vasoactive intestinal polypeptide in rabbit mesenteric artery. / Itoh, T.; Sasaguri, Toshiyuki; Makita, Y.
In: American Journal of Physiology - Heart and Circulatory Physiology, Vol. 18, No. 2, 01.01.1985.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Mechanisms of vasodilation induced by vasoactive intestinal polypeptide in rabbit mesenteric artery
AU - Itoh, T.
AU - Sasaguri, Toshiyuki
AU - Makita, Y.
PY - 1985/1/1
Y1 - 1985/1/1
N2 - 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.
AB - 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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M3 - Article
C2 - 2992292
AN - SCOPUS:18244418933
VL - 18
JO - American Journal of Physiology
JF - American Journal of Physiology
SN - 0363-6135
IS - 2
ER -