ArticlePflugers Archiv : European journal of physiology1989
Potassium channel openers act through an activation of ATP-sensitive K+ channels in guinea-pig cardiac myocytes.
Article in Pflugers Archiv : European journal of physiology, 1989. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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27 citing papers in PubMed, 114 citations in OpenAlex.
- Drug-induced QT interval shortening: potential harbinger of proarrhythmia and regulatory perspectives.British journal of pharmacology · 2010Review
- Predicting drug-induced changes in QT interval and arrhythmias: QT-shortening drugs point to gaps in the ICHS7B Guidelines.British journal of pharmacology · 2008Article
- Cardiac repolarisation and drug regulation: assessing cardiac safety 10 years after the CPMP guidance.Drug safety · 2007Review
- ATP-sensitive potassium channels are altered in ventricular myocytes from diabetic rats.Molecular and cellular biochemistry · 1996Article
- Mechanism of action of K channel openers on skeletal muscle KATP channels. Interactions with nucleotides and protons.The Journal of general physiology · 1996Article
- Action potential duration and force-frequency relationship in isolated rabbit, guinea pig and rat cardiac muscle.Journal of comparative physiology. B, Biochemical, systemic, and environmental physiology · 1996Article
- Time-dependent fading of the activation of KATP channels, induced by aprikalim and nucleotides, in excised membrane patches from cardiac myocytes.British journal of pharmacology · 1995Article
- SR47063, a potent channel opener, activates KATP and a time-dependent current likely due to potassium accumulation.The Journal of membrane biology · 1994Article
- The effect of glibenclamide on frog skeletal muscle: evidence for K+ATP channel activation during fatigue.The Journal of physiology · 1994Article
- K channel openers activate different K channels in vascular smooth muscle cells.Cardiovascular drugs and therapy · 1993Review
- ATP-sensitive K+ channels in cardiac ischemia: an endogenous mechanism for protection of the heart.Cardiovascular drugs and therapy · 1993Article
- Regulation of arterial tone by calcium-dependent K+ channels and ATP-sensitive K+ channels.Cardiovascular drugs and therapy · 1993Review
- Activation and reactivation of the ATP-sensitive K+ channel of the heart can be modified by drugs.Cardiovascular drugs and therapy · 1993Article
- Mechanism of activation of K+ channels by minoxidil-sulfate in Madin-Darby canine kidney cells.The Journal of membrane biology · 1993Article
- Contribution of potassium accumulation in narrow extracellular spaces to the genesis of nicorandil-induced large inward tail current in guinea-pig ventricular cells.Pflugers Archiv : European journal of physiology · 1993Article
- Role of ATP-sensitive K+ channels during anoxia: major differences between rat (newborn and adult) and turtle neurons.The Journal of physiology · 1992Article
- Guanosine diphosphate activates an adenosine 5'-triphosphate-sensitive K+ channel in the rabbit portal vein.The Journal of physiology · 1991Article
- Antagonism of relaxin by glibenclamide in the uterus of the rat in vivo.British journal of pharmacology · 1991Article
- ATP-dependent potassium channels of muscle cells: their properties, regulation, and possible functions.Journal of bioenergetics and biomembranes · 1991Review
- Coenzyme Q10 attenuates cyanide-activation of the ATP-sensitive K+ channel current in single cardiac myocytes of the guinea-pig.Naunyn-Schmiedeberg's archives of pharmacology · 1991Article
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In a previous article (Escande et al. 1988a), we have shown that cromakalim (BRL 34915), a potassium channel opener (PCO), is a potent activator of ATP-sensitive K+ channels in cardiac cells. In the present article, the influence on K+ channels of two other potassium channel openers chemically unrelated to cromakalim, RP 49356 and pinacidil, has been investigated in patch-clamped isolated cardiac myocytes. In the whole-cell configuration, K+ currents were recorded in the presence of 50 microM TTX and 3 microM nitrendipine or 3 mM cobalt. Like cromakalim, RP 49356 or pinacidil activated a time-independent outward current at 33-35 degrees C but not at 19-21 degrees C, which showed little voltage-dependency in the potential range -60 to +60 mV. Its amplitude was a function of the agonist concentration, e.g. it was 2.1 +/- 0.4 nA at +60 mV with 30 microM RP 49356 and 4.3 +/- 0.8 nA with 300 microM. In control conditions, glibenclamide, a blocker of K+-ATP channels in pancreatic and heart cells, affected neither the inward rectifier, iK1, nor the delayed K+ current, iK. At 3 microM, glibenclamide fully prevented the effects of 300 microM RP 49356 or pinacidil. At lower concentrations, glibenclamide partially counteracted the activation by PCOs of a K+ current. In the cell-attached configuration, externally applied RP 49356 or pinacidil caused opening of large channels which reversed around O mV in a high K+ external medium. In inside-out patches, both RP 49356 or pinacidil activated K+-ATP channels by increasing the time period for which the channels remained in the open state. It is concluded that, like cromakalim, RP 49356 and pinacidil are potent activators of K+-ATP channels in cardiac myocytes.
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