{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,24]],"date-time":"2026-03-24T03:43:25Z","timestamp":1774323805398,"version":"3.50.1"},"reference-count":0,"publisher":"American Physiological Society","issue":"6","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Cell Physiology"],"published-print":{"date-parts":[[1994,6,1]]},"abstract":"<jats:p> The properties and function of Ca(2+)-activated K+ (KCa) and voltage-dependent K+ (IK) currents of rabbit coronary myocytes were studied under whole cell voltage-clamp conditions (22 degrees C). Inhibition of KCa by tetraethylammonium chloride (1-10 mM) or charybdotoxin (50-100 nM) suppressed noisy outward rectifying current elicited by 5-s voltage steps or ramp at potentials &gt; 0 mV, reduced the hump of the biphasic ramp current-voltage relation, and shifted by less than +5 mV the potential at which no net steady-state current is recorded (Enet; index of resting membrane potential). Inhibition of steady-state inward Ca2+ currents [ICa(L)] by nifedipine (1 microM) displaced Enet by -11 mV. Analysis of steady-state voltage dependence of IK supported the existence of a \"window\" current between -50 and 0 mV. 4-Aminopyridine (2 mM) blocked a noninactivating component of IK evoked between -30 and -40 mV, abolished the hump current during ramps, and shifted Enet by more than +15 mV; hump current persisted during 2-min ramp depolarizations and peaked near the maximum overlap of the steady-state activation and inactivation curves of IK (about -22 mV). A threefold rise in extracellular Ca2+ concentration (1.8-5.4 mM) enhanced time-dependent outward K+ current (6.7-fold at +40 mV) and shifted Enet by -30 mV. It is concluded that, under steady-state conditions, IK and ICa(L) play a major role in regulating resting membrane potential at a physiological level of intracellular Ca2+ concentration, with a minor contribution from KCa. However, elevation of intracellular Ca2+ concentration enhances KCa and hyperpolarizes the myocyte to limit Ca2+ entry through ICa(L). <\/jats:p>","DOI":"10.1152\/ajpcell.1994.266.6.c1523","type":"journal-article","created":{"date-parts":[[2017,12,24]],"date-time":"2017-12-24T17:57:39Z","timestamp":1514138259000},"page":"C1523-C1537","source":"Crossref","is-referenced-by-count":76,"title":["Physiological role of Ca(2+)-activated and voltage-dependent K+ currents in rabbit coronary myocytes"],"prefix":"10.1152","volume":"266","author":[{"given":"N.","family":"Leblanc","sequence":"first","affiliation":[{"name":"Division of Cardiovascular Sciences, St. Boniface General HospitalResearch Centre, Winnipeg, Manitoba, Canada."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"X.","family":"Wan","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Sciences, St. Boniface General HospitalResearch Centre, Winnipeg, Manitoba, Canada."}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"P. M.","family":"Leung","sequence":"additional","affiliation":[{"name":"Division of Cardiovascular Sciences, St. Boniface General HospitalResearch Centre, Winnipeg, Manitoba, Canada."}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"24","container-title":["American Journal of Physiology-Cell Physiology"],"original-title":[],"language":"en","link":[{"URL":"https:\/\/journals.physiology.org\/doi\/pdf\/10.1152\/ajpcell.1994.266.6.C1523","content-type":"unspecified","content-version":"vor","intended-application":"similarity-checking"}],"deposited":{"date-parts":[[2024,6,17]],"date-time":"2024-06-17T19:41:11Z","timestamp":1718653271000},"score":1,"resource":{"primary":{"URL":"https:\/\/journals.physiology.org\/doi\/10.1152\/ajpcell.1994.266.6.C1523"}},"subtitle":[],"short-title":[],"issued":{"date-parts":[[1994,6,1]]},"references-count":0,"journal-issue":{"issue":"6","published-print":{"date-parts":[[1994,6,1]]}},"alternative-id":["10.1152\/ajpcell.1994.266.6.C1523"],"URL":"https:\/\/doi.org\/10.1152\/ajpcell.1994.266.6.c1523","relation":{},"ISSN":["0363-6143","1522-1563"],"issn-type":[{"value":"0363-6143","type":"print"},{"value":"1522-1563","type":"electronic"}],"subject":[],"published":{"date-parts":[[1994,6,1]]}}}