Phenylephrine suppresses outward K+ currents in rat atrial myocytes
Autor: | Michelle Lamorgese, M. Kirian, D. R. Van Wagoner |
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Rok vydání: | 1996 |
Předmět: |
Agonist
Male medicine.medical_specialty Physiology medicine.drug_class Neurotoxins Rats Sprague-Dawley Phenylephrine Physiology (medical) Internal medicine medicine Myocyte Animals Patch clamp Diacylglycerol kinase Elapid Venoms Dose-Response Relationship Drug Chemistry Myocardium Electric Conductivity Atrial Function Potassium channel Rats Electrophysiology Dose–response relationship Endocrinology Biophysics Potassium Cardiology and Cardiovascular Medicine medicine.drug |
Zdroj: | The American journal of physiology. 271(3 Pt 2) |
ISSN: | 0002-9513 |
Popis: | The modulation of whole cell K+ currents by the alpha 1-adrenergic agonist, phenylephrine, was studied in isolated rat atrial myocytes by use of perforated-patch whole cell recording techniques. The out ward K+ current in these myocytes consists of two inactivating components (iK,f and iK,s), which differ in the kinetics of inactivation and recovery from inactivation, and a noninactivating component, (iK,ss). Superfusion of these myocytes with 10 microM phenylephrine caused a rapid suppression of iK,ss, with little effect on the other current components. This effect of phenylephrine could be mimicked by exogenous application of 1,2-dioctanoyl-sn-glycerol (20 microM), a membrane-permeant diacylglycerol analogue; however, it was clearly distinct from the effect of 5 nM alpha-dendrotoxin, which selectively suppressed the slowly inactivating current component, iK,s, while having no effect on iK,ss. At a dose of 50 microM, phenylephrine also suppressed iK,s. There was no significant effect of phenylephrine (10 or 50 microM) or alpha-dendrotoxin (5 nM) on the rapidly inactivating current component, iK,f. The kinetic and pharmacological differences between these current components suggest that they represent the activity of distinct K+ channels. |
Databáze: | OpenAIRE |
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