Vascular relaxation induced by C-type natriuretic peptide involves the ca2+/NO-synthase/NO pathway.

<h4>Aims</h4>C-type natriuretic peptide (CNP) and nitric oxide (NO) are endothelium-derived factors that play important roles in the regulation of vascular tone and arterial blood pressure. We hypothesized that NO produced by the endothelial NO-synthase (NOS-3) contributes to the relaxat...

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Autores principales: Fernanda A Andrade, Carolina B A Restini, Marcella D Grando, Leandra N Z Ramalho, Lusiane M Bendhack
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Publicado: Public Library of Science (PLoS) 2014
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spelling oai:doaj.org-article:11521d92ec2e4282ab4e710917ca27422021-11-18T08:21:09ZVascular relaxation induced by C-type natriuretic peptide involves the ca2+/NO-synthase/NO pathway.1932-620310.1371/journal.pone.0095446https://doaj.org/article/11521d92ec2e4282ab4e710917ca27422014-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24787693/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Aims</h4>C-type natriuretic peptide (CNP) and nitric oxide (NO) are endothelium-derived factors that play important roles in the regulation of vascular tone and arterial blood pressure. We hypothesized that NO produced by the endothelial NO-synthase (NOS-3) contributes to the relaxation induced by CNP in isolated rat aorta via activation of endothelial NPR-C receptor. Therefore, the aim of this study was to investigate the putative contribution of NO through NPR-C activation in the CNP induced relaxation in isolated conductance artery.<h4>Main methods</h4>Concentration-effect curves for CNP were constructed in aortic rings isolated from rats. Confocal microscopy was used to analyze the cytosolic calcium mobilization induced by CNP. The phosphorylation of the residue Ser1177 of NOS was analyzed by Western blot and the expression and localization of NPR-C receptors was analyzed by immunohistochemistry.<h4>Key findings</h4>CNP was less potent in inducing relaxation in denuded endothelium aortic rings than in intact ones. L-NAME attenuated the potency of CNP and similar results were obtained in the presence of hydroxocobalamin, an intracellular NO0 scavenger. CNP did not change the phosphorylation of Ser1177, the activation site of NOS-3, when compared with control. The addition of CNP produced an increase in [Ca2+]c in endothelial cells and a decrease in [Ca2+]c in vascular smooth muscle cells. The NPR-C-receptors are expressed in endothelial and adventitial rat aortas.<h4>Significance</h4>These results suggest that CNP-induced relaxation in intact aorta isolated from rats involves NO production due to [Ca2+]c increase in endothelial cells possibly through NPR-C activation expressed in these cells. The present study provides a breakthrough in the understanding of the close relationship between the vascular actions of nitric oxide and CNP.Fernanda A AndradeCarolina B A RestiniMarcella D GrandoLeandra N Z RamalhoLusiane M BendhackPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 9, Iss 5, p e95446 (2014)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Fernanda A Andrade
Carolina B A Restini
Marcella D Grando
Leandra N Z Ramalho
Lusiane M Bendhack
Vascular relaxation induced by C-type natriuretic peptide involves the ca2+/NO-synthase/NO pathway.
description <h4>Aims</h4>C-type natriuretic peptide (CNP) and nitric oxide (NO) are endothelium-derived factors that play important roles in the regulation of vascular tone and arterial blood pressure. We hypothesized that NO produced by the endothelial NO-synthase (NOS-3) contributes to the relaxation induced by CNP in isolated rat aorta via activation of endothelial NPR-C receptor. Therefore, the aim of this study was to investigate the putative contribution of NO through NPR-C activation in the CNP induced relaxation in isolated conductance artery.<h4>Main methods</h4>Concentration-effect curves for CNP were constructed in aortic rings isolated from rats. Confocal microscopy was used to analyze the cytosolic calcium mobilization induced by CNP. The phosphorylation of the residue Ser1177 of NOS was analyzed by Western blot and the expression and localization of NPR-C receptors was analyzed by immunohistochemistry.<h4>Key findings</h4>CNP was less potent in inducing relaxation in denuded endothelium aortic rings than in intact ones. L-NAME attenuated the potency of CNP and similar results were obtained in the presence of hydroxocobalamin, an intracellular NO0 scavenger. CNP did not change the phosphorylation of Ser1177, the activation site of NOS-3, when compared with control. The addition of CNP produced an increase in [Ca2+]c in endothelial cells and a decrease in [Ca2+]c in vascular smooth muscle cells. The NPR-C-receptors are expressed in endothelial and adventitial rat aortas.<h4>Significance</h4>These results suggest that CNP-induced relaxation in intact aorta isolated from rats involves NO production due to [Ca2+]c increase in endothelial cells possibly through NPR-C activation expressed in these cells. The present study provides a breakthrough in the understanding of the close relationship between the vascular actions of nitric oxide and CNP.
format article
author Fernanda A Andrade
Carolina B A Restini
Marcella D Grando
Leandra N Z Ramalho
Lusiane M Bendhack
author_facet Fernanda A Andrade
Carolina B A Restini
Marcella D Grando
Leandra N Z Ramalho
Lusiane M Bendhack
author_sort Fernanda A Andrade
title Vascular relaxation induced by C-type natriuretic peptide involves the ca2+/NO-synthase/NO pathway.
title_short Vascular relaxation induced by C-type natriuretic peptide involves the ca2+/NO-synthase/NO pathway.
title_full Vascular relaxation induced by C-type natriuretic peptide involves the ca2+/NO-synthase/NO pathway.
title_fullStr Vascular relaxation induced by C-type natriuretic peptide involves the ca2+/NO-synthase/NO pathway.
title_full_unstemmed Vascular relaxation induced by C-type natriuretic peptide involves the ca2+/NO-synthase/NO pathway.
title_sort vascular relaxation induced by c-type natriuretic peptide involves the ca2+/no-synthase/no pathway.
publisher Public Library of Science (PLoS)
publishDate 2014
url https://doaj.org/article/11521d92ec2e4282ab4e710917ca2742
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