{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T00:44:05Z","timestamp":1791074645272,"version":"4.1.0"},"reference-count":29,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[2000,10,13]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            \u2014Defective excitation-contraction coupling in heart failure is generally associated with both a reduction in sarcoplasmic reticulum (SR) Ca\n            <jats:sup>2+<\/jats:sup>\n            uptake and a greater dependence on transsarcolemmal Na\n            <jats:sup>+<\/jats:sup>\n            -Ca\n            <jats:sup>2+<\/jats:sup>\n            exchange (NCX) for Ca\n            <jats:sup>2+<\/jats:sup>\n            removal. Although a relative increase in NCX is expected when SR function is impaired, few and contradictory studies have addressed whether there is an absolute increase in NCX activity. The present study examines in detail NCX density and function in left ventricular midmyocardial myocytes isolated from normal or tachycardic pacing\u2013induced failing canine hearts. No change of NCX current density was evident in myocytes from failing hearts when intracellular Ca\n            <jats:sup>2+<\/jats:sup>\n            ([Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            ) was buffered to 200 nmol\/L. However, when [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            was minimally buffered with 50 \u03bcmol\/L indo-1, Ca\n            <jats:sup>2+<\/jats:sup>\n            extrusion via NCX during caffeine application was doubled in failing versus normal cells. In other voltage-clamp experiments in which SR uptake was blocked with thapsigargin, both reverse-mode and forward-mode NCX currents and Ca\n            <jats:sup>2+<\/jats:sup>\n            transport were increased &gt;2-fold in failing cells. These results suggest that, in addition to a relative increase in NCX function as a consequence of defective SR Ca\n            <jats:sup>2+<\/jats:sup>\n            uptake, there is an absolute increase in NCX function that depends on [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            in the failing heart.\n          <\/jats:p>","DOI":"10.1161\/01.res.87.8.690","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:52:16Z","timestamp":1339462336000},"page":"690-698","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":135,"title":["Enhanced Ca\n            <sup>2+<\/sup>\n            -Activated Na\n            <sup>+<\/sup>\n            -Ca\n            <sup>2+<\/sup>\n            Exchange Activity in Canine Pacing-Induced Heart Failure"],"prefix":"10.1161","volume":"87","author":[{"given":"Ion A.","family":"Hobai","sequence":"first","affiliation":[{"name":"From the Institute of Molecular Cardiobiology, Division of Cardiology, Department of Medicine, The Johns Hopkins University, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brian","family":"O\u2019Rourke","sequence":"additional","affiliation":[{"name":"From the Institute of Molecular Cardiobiology, Division of Cardiology, Department of Medicine, The Johns Hopkins University, Baltimore, Md."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","first-page":"235","volume":"87","year":"1992","unstructured":"Beuckelmann DJ, Erdmann E. 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Inhibition by external Cd2+ of Na\/Ca exchange and L-type Ca channel in rabbit ventricular myocytes. Am J Physiol. 1997;272:H2164\u2013H2172.","journal-title":"Am J Physiol"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050866"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1085\/jgp.105.3.403"},{"key":"e_1_3_2_20_2","unstructured":"Hobai IA O\u2019Rourke B. Decreased sarcoplasmic reticulum Ca content accounts for defective excitation-contraction coupling in canine pacing induced heart failure. Circulation. In press. Abstract."},{"key":"e_1_3_2_21_2","doi-asserted-by":"publisher","DOI":"10.1007\/s004240050808"},{"key":"e_1_3_2_22_2","doi-asserted-by":"crossref","unstructured":"Fujioka Y Komeda M Matsuoka S. Stoichiometry of Na+-Ca2+ exchange in inside-out patches excised from guinea-pig ventricular myocytes. J Physiol (Lond). 2000;523(pt 2):339\u2013351.","DOI":"10.1111\/j.1469-7793.2000.t01-2-00339.x"},{"key":"e_1_3_2_23_2","doi-asserted-by":"crossref","unstructured":"Egger M Niggli E. Paradoxical block of the Na+-Ca2+ exchanger by extracellular protons in guinea-pig ventricular myocytes. J Physiol (Lond). 2000;523(pt 2):353\u2013366.","DOI":"10.1111\/j.1469-7793.2000.t01-1-00353.x"},{"key":"e_1_3_2_24_2","doi-asserted-by":"publisher","DOI":"10.1161\/res.87.7.581"},{"key":"e_1_3_2_25_2","unstructured":"Sipido KR Volders PGA de Groot SHM Vos MA. Enhanced contractile performance and sarcoplasmic reticulum Ca release in dogs with chronic complete atrio-ventricular block. Circulation. 1998;98(suppl I):I-141. 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