Linked Life Data

10710367

Source:http://linkedlifedata.com/resource/pubmed/id/10710367

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
2000-4-7
pubmed:abstractText
To study the role of endothelial nitric oxide synthase (eNOS) in cardiac function, we compared eNOS expression, contractility, and relaxation in the left ventricles of wild-type and eNOS-deficient mice. eNOS immunostaining is localized to the macro- and microvascular endothelium throughout the myocardium in wild-type mice and is absent in eNOS-/- mice. Whereas blood pressure is elevated in eNOS-/- mice, baseline cardiac contractility (dP/dt(max)) is similar in wild-type and eNOS-/- mice (9,673 +/- 2, 447 and 9,928 +/- 1,566 mmHg/s, respectively). The beta-adrenergic agonist isoproterenol (Iso) at doses of >/=1 ng causes enhanced increases in dP/dt(max) in eNOS-/- mice compared with wild-type controls in vivo (P < 0.01) as well as in Langendorff isolated heart preparations (P < 0.02). beta-Adrenergic receptor binding (B(max)) is not significantly different in the two groups of animals (B(max) = 41.4 +/- 9.4 and 36.1 +/- 5.1 fmol/mg for wild-type and eNOS-/-). Iso-stimulated ventricular relaxation is also enhanced in the eNOS-/- mice, as measured by dP/dt(min) in the isolated heart. However, baseline ventricular relaxation is normal in eNOS-/- mice (tau = 5.2 +/- 1.0 and 5.6 +/- 1.5 ms for wild-type and eNOS-/-, respectively), whereas it is impaired in wild-type mice after NOS inhibition (tau = 8.3 +/- 2.4 ms). cGMP levels in the left ventricle are unaffected by eNOS gene deletion (wild-type: 3.1 +/- 0.8 pmol/mg, eNOS-/-: 3.1 +/- 0.6 pmol/mg), leading us to examine the level of another physiological regulator of cGMP. Atrial natriuretic peptide (ANP) expression is markedly upregulated in the eNOS-/- mice, and exogenous ANP restores ventricular relaxation in wild-type mice treated with NOS inhibitors. These results suggest that eNOS attenuates both inotropic and lusitropic responses to beta-adrenergic stimulation, and it also appears to regulate baseline ventricular relaxation in conjunction with ANP.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0363-6135
pubmed:author
pubmed:issnType
Print
pubmed:volume
278
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
H971-81
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:10710367-Adrenergic beta-Agonists, pubmed-meshheading:10710367-Animals, pubmed-meshheading:10710367-Atrial Natriuretic Factor, pubmed-meshheading:10710367-Blood Pressure, pubmed-meshheading:10710367-Enzyme Inhibitors, pubmed-meshheading:10710367-Female, pubmed-meshheading:10710367-Gene Expression, pubmed-meshheading:10710367-Heart, pubmed-meshheading:10710367-Heart Rate, pubmed-meshheading:10710367-Humans, pubmed-meshheading:10710367-Isoproterenol, pubmed-meshheading:10710367-Male, pubmed-meshheading:10710367-Mice, pubmed-meshheading:10710367-Mice, Inbred C57BL, pubmed-meshheading:10710367-Mice, Knockout, pubmed-meshheading:10710367-Myocardial Contraction, pubmed-meshheading:10710367-Nitric Oxide Synthase, pubmed-meshheading:10710367-Nitric Oxide Synthase Type II, pubmed-meshheading:10710367-Nitric Oxide Synthase Type III, pubmed-meshheading:10710367-Receptors, Adrenergic, beta
pubmed:year
2000
pubmed:articleTitle
Modulation of mouse cardiac function in vivo by eNOS and ANP.
pubmed:affiliation
Cardiovascular Research Center and Cardiology Division, Department of Medicine, Massachusetts General Hospital and Harvard Medical School, Charlestown, Massachusetts 02129, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't