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Muscarinic and beta-adrenergic regulation of heart rate, force of contraction and calcium current is preserved in mice lacking endothelial nitric oxide synthase

1999Journal article Open access
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dc.contributor.authorVandecasteele, Grégoire
dc.contributor.authorEschenhagen, Thomaspt
dc.contributor.authorScholz, Hassopt
dc.contributor.authorStein, Birgittpt
dc.contributor.authorVerde, Ignacio
dc.contributor.authorFischmeister, Rodolphept
dc.date.accessioned2010-04-28T10:06:50Z
dc.date.available2010-04-28T10:06:50Z
dc.date.issued1999
dc.description.abstractNitric oxide (NO) is an ubiquitous signaling molecule produced from L-arginine by NO synthase (NOS). In the vasculature, NO mediates parasympathetic endothelium-dependent vasodilation. NO may also mediate the parasympathetic control of myocardial function1. This is supported by the observations that NOS3, the endothelial constitutive NOS, is expressed in normal cardiac myocytes from rodents2 and human3, and NOS and/or guanylyl cyclase inhibitors antagonize the effect of muscarinic agonists on heart rate4,5, atrio–ventricular conduction6, contractility2,4,7 and L-type calcium current1,2,5,6. Here we examine the autonomic regulation of the heart in genetically engineered mice deficient in NOS3 (NOS3-KO)(ref. 8). We show that the chronotropic and inotropic responses to both β-adrenergic and muscarinic agonists were unaltered in isolated cardiac tissue preparations from NOS3-KO mice, although these mice have a defective parasympathetic regulation of vascular tone8,9. Similarly, β-adrenergic stimulation and muscarinic inhibition of the calcium current did not differ in cardiac myocytes from NOS3-KO mice and those from wild-type mice. RT–PCR did not demonstrate upregulation of other NOS isoforms. Similarly, Gi/Go proteins and muscarinic receptor density were unaltered. These data refute the idea that NOS3 is obligatory for the normal autonomic control of cardiac muscle function10.
dc.identifier.urihttp://hdl.handle.net/10400.6/561
dc.languageeng
dc.titleMuscarinic and beta-adrenergic regulation of heart rate, force of contraction and calcium current is preserved in mice lacking endothelial nitric oxide synthasept
dc.typejournal article
dspace.entity.typePublication
oaire.citation.issue5:331-4pt
oaire.citation.titleNature Medicinept
person.familyNameVandecasteele
person.familyNameVerde
person.givenNameGrégoire
person.givenNameIgnacio
person.identifier.ciencia-idD012-1D7C-791A
person.identifier.orcid0000-0002-4046-4171
person.identifier.orcid0000-0003-3492-5725
person.identifier.ridM-3991-2013
person.identifier.scopus-author-id55913729400
rcaap.rightsopenAccess
rcaap.typearticlept
relation.isAuthorOfPublicationd11a75df-74f0-4cb6-a49a-0ee646ffc342
relation.isAuthorOfPublicationbfb58284-b817-4267-9628-8fa150aa681c
relation.isAuthorOfPublication.latestForDiscoverybfb58284-b817-4267-9628-8fa150aa681c

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