ArticleThe Journal of physiology1997
Modulation of inwardly rectifying potassium channels in cultured bovine pulmonary artery endothelial cells.
Article in The Journal of physiology, 1997. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Functional expression of inwardly rectifying and ATP-sensitive potassium channels in human pulmonary artery smooth muscle and endothelial cells.The Journal of physiology · 2026Article
- Shear-Stress Sensitive Inwardly-Rectifying KCellular physiology and biochemistry : international journal of experimental cellular physiology, biochemistry, and pharmacology · 2019Article
- Boosting the signal: Endothelial inward rectifier KMicrocirculation (New York, N.Y. : 1994) · 2017Review
- Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles.Comprehensive Physiology · 2017Review
- Inward Rectifier K+ Currents Are Regulated by CaMKII in Endothelial Cells of Primarily Cultured Bovine Pulmonary Arteries.PloS one · 2015Article
- SKCa Channels Blockage Increases the Expression of Adenosine A2A Receptor in Jurkat Human T Cells.BioResearch open access · 2013Article
- Hypoxic pulmonary vasoconstriction.Physiological reviews · 2012Review
- Responses of pigeon vestibular hair cells to cholinergic agonists and antagonists.Brain research · 2011Article
- Protein kinase A-dependent biophysical phenotype for V227F-KCNJ2 mutation in catecholaminergic polymorphic ventricular tachycardia.Circulation. Arrhythmia and electrophysiology · 2009Article
- Cholesterol and Kir channels.IUBMB life · 2009Review
- RhoA GTPase and F-actin dynamically regulate the permeability of Cx43-made channels in rat cardiac myocytes.The Journal of biological chemistry · 2008Article
- Regulation of a family of inwardly rectifying potassium channels (Kir2) by the m1 muscarinic receptor and the small GTPase Rho.Pflugers Archiv : European journal of physiology · 2006Article
- Functional expression of inward rectifier potassium channels in cultured human pulmonary smooth muscle cells: evidence for a major role of Kir2.4 subunits.The Journal of membrane biology · 2006Article
- Ion channels and ion transporters of the transverse tubular system of skeletal muscle.Journal of muscle research and cell motility · 2006Review
- Mechanisms underlying regulation of a barium-sensitive K+ conductance by ATP in single proximal tubule cells isolated from frog kidney.The Journal of membrane biology · 2005Article
- Cholesterol sensitivity and lipid raft targeting of Kir2.1 channels.Biophysical journal · 2004Article
- Dopamine modulates inwardly rectifying potassium currents in medial prefrontal cortex pyramidal neurons.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2004Article
- Modulation of endothelial inward-rectifier K+ current by optical isomers of cholesterol.Biophysical journal · 2002Article
- Receptor phosphorylation mediates estradiol reduction of alpha2-adrenoceptor coupling to G protein in the hypothalamus of female rats.Endocrine · 2001Article
- Properties of heterologously expressed hTRP3 channels in bovine pulmonary artery endothelial cells.The Journal of physiology · 1999Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
1. We have used the patch-clamp technique to study modulation of the inwardly rectifying K+ current (IK(IR)) in cultured bovine pulmonary artery endothelial cells (CPAE cells). In whole-cell mode, IK(IR) was defined as the Ba(2+)-sensitive current. In single channel recordings, we observed a strongly inwardly rectifying and K(+)-selective channel with a conductance of 31 +/- 3 pS. 2. Reverse transcriptase-polymerase chain reaction (RT-PCR) analysis and functional data suggest that the endothelial IRK is most probably Kir2.1. 3. Intracellular ATP is required to prevent run-down of IRK in whole-cell mode. Single channel activity disappeared in inside-out patches exposed to ATP-free solution and in cell-attached patches on cells exposed to metabolic inhibition (KCN, 2-deoxyglucose). 4. The non-hydrolysable ATP analogues, ATP gamma S and adenylyl imidodiphosphate (AMP-PNP), did not prevent run-down. Run-down did not occur in the presence of okadaic acid, a phosphatase inhibitor, but was enhanced in the presence of protamine, an activator of phosphatase 2A (PP2A). 5. GTP gamma S and AlF4- inhibited IRK, also in the presence of ATP. GTP beta S antagonized the GTP gamma S effect. Pretreatment of the cells with PTX did not affect the GTP gamma S-induced inhibition. Okadaic acid, however, slowed this inhibition. 6. Neither activation of protein kinase A (PKA) nor activation of protein kinase C (PKC) affected IRK. Additionally, neither cytochalasin B nor a high concentration of intracellular Ca2+ affected the time course of IRK run-down. 7. We conclude that run-down of IRK is probably due to dephosphorylation by PP2A. Activation of a PTX-insensitive G protein inhibits this current by a mechanism that is neither mediated via the PKA and PKC pathways nor by intracellular Ca2+, but supposedly by a G protein-dependent activation of a phosphatase.
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