ArticleThe Journal of physiology2005
The nitric oxide donor sodium nitroprusside stimulates the Na+-K+ pump in isolated rabbit cardiac myocytes.
Article in The Journal of physiology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed, 50 citations in OpenAlex.
- N-acetylcysteine attenuates the decline in muscle Na+,K+-pump activity and delays fatigue during prolonged exercise in humans.The Journal of physiology · 2006Trial
- Hypoxic Stress-Dependent Regulation of Na,K-ATPase in Ischemic Heart Disease.International journal of molecular sciences · 2023Review
- Local tissue manipulation via a force- and pressure-controlled AFM micropipette for analysis of cellular processes.Scientific reports · 2018Article
- Inhibition of endothelial nitric oxide synthase decreases breast cancer cell MDA-MB-231 adhesion to intact microvessels under physiological flows.American journal of physiology. Heart and circulatory physiology · 2016Article
- Nicorandil stimulates a Na⁺/Ca²⁺ exchanger by activating guanylate cyclase in guinea pig cardiac myocytes.Pflugers Archiv : European journal of physiology · 2016Article
- Stimulation of the cardiac myocyte Na+-K+ pump due to reversal of its constitutive oxidative inhibition.American journal of physiology. Cell physiology · 2015Article
- Triggers, inhibitors, mechanisms, and significance of eryptosis: the suicidal erythrocyte death.BioMed research international · 2015Review
- Oxidative inhibition of the vascular Na+-K+ pump via NADPH oxidase-dependent β1-subunit glutathionylation: implications for angiotensin II-induced vascular dysfunction.Free radical biology & medicine · 2013Article
- Nitric oxide regulates cardiac intracellular Na⁺ and Ca²⁺ by modulating Na/K ATPase via PKCε and phospholemman-dependent mechanism.Journal of molecular and cellular cardiology · 2013Article
- Protein kinase-dependent oxidative regulation of the cardiac Na+-K+ pump: evidence from in vivo and in vitro modulation of cell signalling.The Journal of physiology · 2013Article
- Regulation of the cardiac sodium pump.Cellular and molecular life sciences : CMLS · 2013Review
- Susceptibility of β1 Na+-K+ pump subunit to glutathionylation and oxidative inhibition depends on conformational state of pump.The Journal of biological chemistry · 2012Article
- Ouabain increases iNOS-dependent nitric oxide generation which contributes to the hypertrophic effect of the glycoside: possible role of peroxynitrite formation.Molecular and cellular biochemistry · 2012Article
- Phospholemman Ser69 phosphorylation contributes to sildenafil-induced cardioprotection against reperfusion injury.American journal of physiology. Heart and circulatory physiology · 2010Article
- Phospholemman: a novel cardiac stress protein.Clinical and translational science · 2010Review
- Activation of cAMP-dependent signaling induces oxidative modification of the cardiac Na+-K+ pump and inhibits its activity.The Journal of biological chemistry · 2010Article
- Inhibition of suicidal erythrocyte death by nitric oxide.Pflugers Archiv : European journal of physiology · 2008Article
- Nitric oxide mediates the vagal protective effect on ventricular fibrillation via effects on action potential duration restitution in the rabbit heart.The Journal of physiology · 2007Article
- Beta3-adrenoceptor agonist stimulation of the Na+, K+ -pump in rat skeletal muscle is mediated by beta2- rather than beta3-adrenoceptors.British journal of pharmacology · 2006Article
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Nitric oxide (NO) affects the membrane Na(+)-K(+) pump in a tissue-dependent manner. Stimulation of intrinsic pump activity, stimulation secondary to NO-induced Na(+) influx into cells or inhibition has been reported. We used the whole-cell patch clamp technique to measure electrogenic Na(+)-K(+) pump current (I(p)) in rabbit ventricular myocytes. Myocytes were voltage clamped with wide-tipped patch pipettes to achieve optimal perfusion of the intracellular compartment, and I(p) was identified as the shift in holding current induced by 100 microm ouabain. The NO donor sodium nitroprusside (SNP) in concentrations of 1, 10, 50 or 100 microm induced a significant increase in I(p) when the intracellular compartment was perfused with pipette solutions containing 10 mm Na(+), a concentration near physiological levels. SNP had no effect when the pump was near-maximally activated by 80 mm Na(+) in pipette solutions. Stimulation persisted in the absence of extracellular Na(+), indicating its independence of transmembrane Na(+) influx. The SNP-induced pump stimulation was abolished by inhibition of soluble guanylyl cyclase (sGC) with 1H-[1,2,4]oxadiazole[4,3-a]quinoxalin-1-one, by inhibition of protein kinase G (PKG) with KT-5823 or by inhibition of protein phosphatase with okadaic acid. Inclusion of the non-hydrolysable cGMP analogue 8pCPT-cGMP, activated recombinant PKG or the sGC-activator YC-1 in patch pipette filling solutions reproduced the SNP-induced pump stimulation. Pump stimulation induced by YC-1 was dependent on the Na(+) concentration but not the K(+) concentration in pipette filling solutions, suggesting an altered sensitivity of the Na(+)-K(+) pump to intracellular Na(+).
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.