{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,11]],"date-time":"2026-03-11T17:03:27Z","timestamp":1773248607593,"version":"3.50.1"},"reference-count":0,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[1994,1,1]],"date-time":"1994-01-01T00:00:00Z","timestamp":757382400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[1994,1]]},"abstract":"<jats:p>1. To address the questions of whether beta\u2010adrenoreceptor stimulation can augment ATP\u2010sensitive potassium current (IK(ATP)), and what the mechanism of such an effect might be, action potentials and whole\u2010cell ionic currents were recorded from adult cat cardiac ventricular myocytes using a conventional whole\u2010cell patch technique. 2. An outwardly directed, ohmic, non\u2010inactivating, glyburide (10 microM)\u2010sensitive current reversing near the reversal potential for potassium (EK) developed slowly (10\u201025 min) in cells dialysed with an ATP\u2010free pipette (intracellular) solution. During this time, action potential duration markedly decreased while the resting membrane potential hyperpolarized closer to EK. Extended (&gt; 30 min) periods of internal dialysis with ATP\u2010free solution eventually resulted in run\u2010down of the outward current. 3. Externally applied isoprenaline (1 microM) caused a rapidly developing (&lt; or = 60 s), sustained enhancement of a glyburide (10 microM)\u2010sensitive IK(ATP) in cells internally dialysed with ATP\u2010free solution. IK(ATP) remained elevated even after the isoprenaline was removed, and subsequent applications of the beta\u2010agonist failed to increase IK(ATP) further. Half\u2010maximal isoprenaline stimulation of IK(ATP) occurred at a concentration of approximate of 1.5 nM. 4. Pretreatment with propranolol (1 microM) prevented the enhancement of IK(ATP) by a beta\u2010agonist. 5. Isoprenaline\u2010induced IK(ATP) could be blocked by either internal application of GDP\u2010beta\u2010S (2\u20105 mM) or pretreatment with cholera toxin (1\u201010 microgram ml\u20101, &gt; 18 h). Pretreatment with pertussis toxin (1\u20102 microgram ml\u20101, &gt; 18 h) did not attenuate the isoprenaline response, whereas internally applied GTP\u2010gamma\u2010S (100 microM) or F\u2010 (20 mM) caused IK(ATP) to increase rapidly in the absence of the beta\u2010agonist. 6. Although externally applied forskolin (10 microM) also stimulated IK(ATP), neither 1,9\u2010dideoxyforskolin (10 microM) nor 8\u2010(4\u2010chlorophenylthio)\u2010cAMP (200 microM) had any effect on the current. Internal application of the adenylate cyclase inhibitor 2'\u2010deoxyadenosine\u20103'\u2010monophosphate (100 microM) resulted in a reduction in the response to isoprenaline, while internal application of a protein kinase A inhibitor (PKI5\u201024, 22.5 microM) did not attenuate the response to the beta\u2010agonist. 7. IK(ATP) developed slowly during internal dialysis with ATP\u2010free solution.(ABSTRACT TRUNCATED AT 400 WORDS)<\/jats:p>","DOI":"10.1113\/jphysiol.1994.sp020008","type":"journal-article","created":{"date-parts":[[2014,12,17]],"date-time":"2014-12-17T13:06:43Z","timestamp":1418821603000},"page":"131-145","source":"Crossref","is-referenced-by-count":42,"title":["Enhancement of ATP\u2010sensitive potassium current in cat ventricular myocytes by beta\u2010adrenoreceptor stimulation."],"prefix":"10.1113","volume":"474","author":[{"given":"T E","family":"Schackow","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"R E","family":"Ten Eick","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"311","published-online":{"date-parts":[[1994,1]]},"container-title":["The Journal of Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/api.wiley.com\/onlinelibrary\/tdm\/v1\/articles\/10.1113%2Fjphysiol.1994.sp020008","content-type":"unspecified","content-version":"vor","intended-application":"text-mining"},{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/pdf\/10.1113\/jphysiol.1994.sp020008","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2023,10,24]],"date-time":"2023-10-24T00:01:58Z","timestamp":1698105718000},"score":1,"resource":{"primary":{"URL":"https:\/\/physoc.onlinelibrary.wiley.com\/doi\/10.1113\/jphysiol.1994.sp020008"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,1]]},"references-count":0,"journal-issue":{"issue":"1","published-print":{"date-parts":[[1994,1]]}},"alternative-id":["10.1113\/jphysiol.1994.sp020008"],"URL":"https:\/\/doi.org\/10.1113\/jphysiol.1994.sp020008","archive":["Portico"],"relation":{},"ISSN":["0022-3751","1469-7793"],"issn-type":[{"value":"0022-3751","type":"print"},{"value":"1469-7793","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,1]]}}}