Mechanisms associated to impaired activity of cardiac P-type ATPases in endothelial nitric oxide synthase knockout mice-Reference-Cited by-同舟云学术

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Mechanisms associated to impaired activity of cardiac P-type ATPases in endothelial nitric oxide synthase knockout mice

Published:2012-08-09 Issue:2 Volume:69 Page:207-214
ISSN:1138-7548
Container-title:Journal of Physiology and Biochemistry
language:en
Short-container-title:J Physiol Biochem

Author:

Rezende Daniele C.,Pôças Elisa S. C.,Muzi-Filho Humberto,Cunha Valéria M. N.,Caricati-Neto Afonso,Jurkiewicz Aron,Noël François,Quintas Luis E. M.

Publisher

Springer Science and Business Media LLC

Subject

General Medicine,Biochemistry,Physiology

Link

http://link.springer.com/content/pdf/10.1007/s13105-012-0203-x.pdf

Reference44 articles.

1. Ait-Mamar B, Cailleret M, Rucker-Martin C et al (2005) The cytosolic phospholipase A2 pathway, a safeguard of β2-adrenergic cardiac effects in rat. J Biol Chem 280:18881–18890

2. Bambrick LL, Howlett EE, Feng ZP et al (1988) Radioligand binding to muscle homogenates to quantify receptor and ion channel numbers. J Pharmacol Methods 20:313–321

3. Barreto F, Rezende DC, Scaramello CB et al (2010) Lack of evidence for regulation of cardiac P-type ATPases and MAP kinases in transgenic mice with cardiac-specific overexpression of constitutively active α1B-adrenoceptors. Braz J Med Biol Res 43:500–505

4. Barouch LA, Harrison RW, Skaf MW et al (2002) Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms. Nature 416:337–339

5. Bartunek J, Weinberg EO, Tajima M et al (2000) Chronic N(G)-nitro-l-arginine methyl ester-induced hypertension: novel molecular adaptation to systolic load in absence of hypertrophy. Circulation 101:423–429

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