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Vasoactive intestinal polypeptide relaxes isolated rat pulmonary artery rings through two distinct mechanisms.

Authors: Zhang, S  Liu, Y  Guo, S  Zhang, J  Chu, X  Jiang, C  Zhu, D 
Citation: Zhang S, etal., J Physiol Sci. 2010 Nov;60(6):389-97. Epub 2010 Aug 7.
Pubmed: (View Article at PubMed) PMID:20694540
DOI: Full-text: DOI:10.1007/s12576-010-0107-x

Vasoactive intestinal polypeptide (VIP), an endogenous neuropeptide normally present in lungs and other organs, relaxes pulmonary arteries (PAs) in different species, whereas the underlying mechanisms are still not fully understood. The aim of this study, therefore, is to investigate the signal transduction of VIP in the relaxation of isolated rat PA rings. The isometric tension of the rings was studied in vitro with force-electricity transducers. In endothelium-intact (EI) rings, VIP elicited concentration-dependent relaxation after the rings were pre-contracted by phenylephrine. A similar effect, though smaller, was observed in endothelium-denuded (ED) rings. Inhibition of the endothelial nitric oxide synthase (eNOS) by NG-nitro-L-arginine methyl ester diminished the VIP-induced vasodilatation of PA rings. The VIP-induced vasorelaxation was markedly reduced by the inhibition of the phosphatidylinositol 3-kinase/protein kinase B (PI3K/Akt) signaling pathway with wortmannin and LY294002, respectively, which was seen in EI rings, but not in ED rings. Western blot analysis revealed that VIP increased the phosphorylation of eNOS at Ser 1177, but did not affect the overall expression of eNOS. In ED rings, the PKA inhibitor H-89 and K(ATP) channel inhibitor glibenclamide almost totally abolished the vasodilatation effect of VIP. The results suggested that the vasodilatation effect of VIP on rat PAs is mediated by both vascular endothelium and smooth muscle, involving respectively the PI3K/Akt-eNOS pathway and the PKA-K(ATP) channel pathway.


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CRRD Object Information
CRRD ID: 5685631
Created: 2012-01-12
Species: All species
Last Modified: 2012-01-12
Status: ACTIVE


RGD is funded by grant HL64541 from the National Heart, Lung, and Blood Institute on behalf of the NIH.