The α2 isoform Na,K-ATPase modulates contraction of rat mesenteric small artery via cSrc-dependent Ca2+ sensitization

Author:

Bouzinova E. V.1,Hangaard L.1,Staehr C.1,Mazur A.1,Ferreira A.1,Chibalin A. V.2,Sandow S. L.3,Xie Z.4,Aalkjaer C.1,Matchkov V. V.1ORCID

Affiliation:

1. Department of Biomedicine; Aarhus University; Aarhus C Denmark

2. Department of Molecular Medicine and Surgery; Integrative Physiology; Karolinska Institutet; Stockholm Sweden

3. Faculty of Science, Health, Education and Engineering; University of the Sunshine Coast; Maroochydore Qld Australia

4. Marshall Institute for Interdisciplinary Research; Marshall University; Huntington WV USA

Funder

Sundhed og Sygdom, Det Frie Forskningsråd

Novo Nordisk Fonden

Lundbeckfonden

Brain Foundation

Publisher

Wiley

Subject

Physiology

Reference82 articles.

1. Isozymes of the Na-K-ATPase: heterogeneity in structure, diversity in function;Blanco;Am J Physiol,1998

2. Specialized functional diversity and interactions of the Na,K-ATPase;Matchkov;Front Physiol,2016

3. Nanomolar ouabain increases NCX1 expression and enhances Ca2+ signaling in human arterial myocytes: a mechanism that links salt to increased vascular resistance?;Linde;Am J Physiol,2012

4. Clearance of store-released Ca2+ by the Na+-Ca2+ exchanger is diminished in aortic smooth muscle from Na+-K+-ATPase alpha 2-isoform gene-ablated mice;Lynch;Am J Physiol,2008

5. Signaling mechanisms that link salt retention to hypertension: endogenous ouabain, the Na+ pump, the Na+/Ca2+ exchanger and TRPC proteins;Blaustein;Biochim Biophys Acta,1802

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