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Cyclic AMP relaxation of rat aortic smooth muscle is mediated in part by decrease of depletion of intracellular Ca(2+) stores and inhibition of capacitative calcium entry.

Abstract：

:Despite a large number of studies, the mechanism by which 3',5'-cyclic monophosphate (cAMP) induces vasorelaxation is not fully understood. The comparison between results obtained in different vessels or species has often been the source of conflicting reports. In order to shed more light onto this mechanism, we studied the effects of forskolin in phenylephrine-pre-contracted endothelium-denuded rat aorta and measured cAMP levels in rat aortic myocytes by enzyme-immunoassay. Nanomolar forskolin relaxed phenylephrine-induced contractions. This effect was mimicked by dibutyryl-cAMP and was potentiated by rolipram or a p38-mitogen-activated protein kinase (p38-MAPK) inhibitor (SB-203580). Nifedipine and verapamil partially relaxed phenylephrine-induced contractions, while further application of cAMP-elevating agents fully relaxed these contractions. In Ca(2+)-free extracellular solution, forskolin reduced phenylephrine-induced transient contractions and reduced the Ca(2+)-induced contraction after depletion of intracellular stores. Nanomolar concentrations of forskolin increased basal cAMP levels only in the presence of rolipram or phenylephrine, which did not modify intracellular levels of cAMP by themselves. In conclusion, relaxation by cAMP is mediated in part by decrease of depletion of intracellular Ca(2+) stores and inhibition of capacitative calcium entry. This study provides the first evidence that inhibition of PDE4 or p38-MAPK potentiates the vasodilator effect of cAMP-elevating agents in rat aortic myocytes.

journal_name

Vascul Pharmacol

journal_title

Vascular pharmacology

authors

Cuíñas A,Elíes J,Orallo F,Campos-Toimil M

doi

10.1016/j.vph.2012.08.007

subject

Has Abstract

pub_date

2013-01-01 00:00:00

pages

98-104

issue

1-2

eissn

1537-1891

issn

1879-3649

pii

S1537-1891(12)00183-8

journal_volume

58

pub_type

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