{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,8,31]],"date-time":"2026-08-31T11:22:21Z","timestamp":1788175341252,"version":"build-2803163510"},"reference-count":55,"publisher":"American Physiological Society","issue":"2","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[1998,8,1]]},"abstract":"<jats:p>The translocation mechanisms involved in the \u03b1<jats:sub>1<\/jats:sub>-adrenoceptor-stimulated efflux of the potassium analog<jats:sup>86<\/jats:sup>Rb<jats:sup>+<\/jats:sup>were studied in isolated rat hearts. Phenylephrine (in the presence of a \u03b2-blocker) increased the efflux of<jats:sup>86<\/jats:sup>Rb<jats:sup>+<\/jats:sup>and<jats:sup>42<\/jats:sup>K<jats:sup>+<\/jats:sup>, and the Na-K-2Cl (or K-Cl) cotransport inhibitor bumetanide reduced the response by 42 \u00b1 11%. Furosemide inhibited the response with a lower potency than that of bumetanide. The bumetanide-insensitive efflux was largely sensitive to the K<jats:sup>+<\/jats:sup>channel inhibitor 4-aminopyridine. Inhibitors of the Na<jats:sup>+<\/jats:sup>\/H<jats:sup>+<\/jats:sup>exchanger or the Na<jats:sup>+<\/jats:sup>-K<jats:sup>+<\/jats:sup>pump had no effect on the increased<jats:sup>86<\/jats:sup>Rb<jats:sup>+<\/jats:sup>efflux. The activation of the Na-K-2Cl cotransporter was dependent on the extracellular signal-regulated kinase (ERK) subgroup of the mitogen-activated protein (MAP) kinase family. Phenylephrine stimulation increased ERK activity 3.4-fold. PD-98059, an inhibitor of the ERK cascade, reduced both the increased<jats:sup>86<\/jats:sup>Rb<jats:sup>+<\/jats:sup>efflux and ERK activity. Specific inhibitors of protein kinase C and Ca<jats:sup>2+<\/jats:sup>\/calmodulin-dependent kinase II had no effect. In conclusion, \u03b1<jats:sub>1<\/jats:sub>-adrenoceptor stimulation increases<jats:sup>86<\/jats:sup>Rb<jats:sup>+<\/jats:sup>efflux from the rat heart via K<jats:sup>+<\/jats:sup>channels and a Na-K-2Cl cotransporter. 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