{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,2]],"date-time":"2026-10-02T09:38:56Z","timestamp":1790933936827,"version":"4.1.0"},"reference-count":49,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"2","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["Circulation Research"],"published-print":{"date-parts":[[1995,8]]},"abstract":"<jats:p>\n            <jats:italic>Abstract<\/jats:italic>\n            The membrane potential (E\n            <jats:sub>m<\/jats:sub>\n            ) of pulmonary arterial smooth muscle cells (PASMCs) regulates pulmonary arterial tone by controlling voltage-gated Ca\n            <jats:sup>2+<\/jats:sup>\n            channel activity, which is a major contributor to [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            . The resting membrane is mainly permeable to K\n            <jats:sup>+<\/jats:sup>\n            ; thus, the resting E\n            <jats:sub>m<\/jats:sub>\n            is controlled by K\n            <jats:sup>+<\/jats:sup>\n            permeability through sarcolemmal K\n            <jats:sup>+<\/jats:sup>\n            channels. At least three K\n            <jats:sup>+<\/jats:sup>\n            currents, voltage-gated K\n            <jats:sup>+<\/jats:sup>\n            (K\n            <jats:sub>V<\/jats:sub>\n            ) currents, Ca\n            <jats:sup>2+<\/jats:sup>\n            -activated K\n            <jats:sup>+<\/jats:sup>\n            (K\n            <jats:sub>Ca<\/jats:sub>\n            ) currents, and ATP-sensitive (K\n            <jats:sub>ATP<\/jats:sub>\n            ) currents, have been identified in PASMCs. In this study, both patch-clamp and quantitative fluorescent microscopy techniques were used to determine which kind(s) of K\n            <jats:sup>+<\/jats:sup>\n            channels (K\n            <jats:sub>V<\/jats:sub>\n            , K\n            <jats:sub>Ca<\/jats:sub>\n            , and\/or K\n            <jats:sub>ATP<\/jats:sub>\n            ) is responsible for controlling E\n            <jats:sub>m<\/jats:sub>\n            and [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            under resting conditions in rat PASMCs. When the bath solution contained 1.8 mmol\/L Ca\n            <jats:sup>2+<\/jats:sup>\n            and the pipette solution included 0.1 mmol\/L EGTA, depolarizations (\u221240 to +80 mV) elicited both K\n            <jats:sub>Ca<\/jats:sub>\n            and K\n            <jats:sub>V<\/jats:sub>\n            currents. Removal of extracellular Ca\n            <jats:sup>2+<\/jats:sup>\n            and increase of intracellular EGTA concentration (to 10 mmol\/L) eliminated the Ca\n            <jats:sup>2+<\/jats:sup>\n            influx\u2013dependent K\n            <jats:sub>Ca<\/jats:sub>\n            current. 4-Aminopyridine (4-AP, 5 to 10 mmol\/L) but not charybdotoxin (ChTX, 10 to 20 nmol\/L) significantly reduced K\n            <jats:sub>V<\/jats:sub>\n            current under these conditions. In current-clamp experiments, 4-AP decreased E\n            <jats:sub>m<\/jats:sub>\n            (depolarization) and induced Ca\n            <jats:sup>2+<\/jats:sup>\n            -dependent action potentials; this depolarization increased [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            in intact PASMCs. Neither ChTX nor the specific blocker of K\n            <jats:sub>ATP<\/jats:sub>\n            channels, glibenclamide (2 to 10 \u03bcmol\/L), caused membrane depolarization and the increase in [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            . However, pretreatment of PASMCs with ChTX enhanced the 4-AP\u2013induced increase in [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            . These results suggest that the 4-AP\u2013sensitive K\n            <jats:sub>V<\/jats:sub>\n            currents that are active in the resting state are the major contributors to regulation of E\n            <jats:sub>m<\/jats:sub>\n            and thus [Ca\n            <jats:sup>2+<\/jats:sup>\n            ]\n            <jats:sub>i<\/jats:sub>\n            in rat PASMCs.\n          <\/jats:p>","DOI":"10.1161\/01.res.77.2.370","type":"journal-article","created":{"date-parts":[[2012,6,12]],"date-time":"2012-06-12T00:47:05Z","timestamp":1339462025000},"page":"370-378","update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":249,"title":["Voltage-Gated K\n            <sup>+<\/sup>\n            Currents Regulate Resting Membrane Potential and [Ca\n            <sup>2+<\/sup>\n            ]\n            <sub>i<\/sub>\n            in Pulmonary Arterial Myocytes"],"prefix":"10.1161","volume":"77","author":[{"given":"Xiao-Jian","family":"Yuan","sequence":"first","affiliation":[{"name":"From the Department of Medicine, Division of Pulmonary and Critical Care Medicine, and the Department of Physiology, University of Maryland School of Medicine, Baltimore."}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"276","reference":[{"key":"e_1_3_2_1_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1990.259.1.C3"},{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1995.268.4.C799"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1152\/ajpcell.1992.262.4.C916"},{"key":"e_1_3_2_4_2","first-page":"H365","volume":"266","year":"1994","unstructured":"Smirnov SV, Robertson TP, Ward JPT, Aaronson PI. 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