{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T22:15:02Z","timestamp":1790892902439,"version":"4.1.0"},"reference-count":75,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Renal Physiology"],"published-print":{"date-parts":[[2007,7]]},"abstract":"<jats:p>\n                    Apical low-conductance SK and high-conductance Ca\n                    <jats:sup>2+<\/jats:sup>\n                    -activated BK channels are present in distal nephron, including the cortical collecting duct (CCD). Flow-stimulated net K secretion ( J\n                    <jats:sub>K<\/jats:sub>\n                    ) in the CCD is 1) blocked by iberiotoxin, an inhibitor of BK but not SK channels, and 2) associated with an increase in [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    , leading us to conclude that BK channels mediate flow-stimulated J\n                    <jats:sub>K<\/jats:sub>\n                    . To examine the Ca\n                    <jats:sup>2+<\/jats:sup>\n                    dependence and sources of Ca\n                    <jats:sup>2+<\/jats:sup>\n                    contributing to flow-stimulated J\n                    <jats:sub>K<\/jats:sub>\n                    , J\n                    <jats:sub>K<\/jats:sub>\n                    and net Na absorption ( J\n                    <jats:sub>Na<\/jats:sub>\n                    ) were measured at slow (\u223c1) and fast (\u223c5 nl\u00b7min\n                    <jats:sup>\u22121<\/jats:sup>\n                    \u00b7mm\n                    <jats:sup>\u22121<\/jats:sup>\n                    ) flow rates in rabbit CCDs microperfused in the absence of luminal Ca\n                    <jats:sup>2+<\/jats:sup>\n                    or after pretreatment with BAPTA-AM to chelate intracellular Ca\n                    <jats:sup>2+<\/jats:sup>\n                    , 2-aminoethoxydiphenyl borate (2-APB), to inhibit the inositol 1,4,5-trisphosphate (IP\n                    <jats:sub>3<\/jats:sub>\n                    ) receptor or thapsigargin to deplete internal stores. These treatments, which do not affect flow-stimulated J\n                    <jats:sub>Na<\/jats:sub>\n                    (Morimoto et al. Am J Physiol Renal Physiol 291: F663\u2013F669, 2006), inhibited flow-stimulated J\n                    <jats:sub>K<\/jats:sub>\n                    . Increases in [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    stimulate exocytosis. To test whether flow induces exocytic insertion of preformed BK channels into the apical membrane, CCDs were pretreated with 10 \u03bcM colchicine (COL) to disrupt microtubule function or 5 \u03bcg\/ml brefeldin-A (BFA) to inhibit delivery of channels from the intracellular pool to the plasma membrane. Both agents inhibited flow-stimulated J\n                    <jats:sub>K<\/jats:sub>\n                    but not J\n                    <jats:sub>Na<\/jats:sub>\n                    (Morimoto et al. Am J Physiol Renal Physiol 291: F663\u2013F669, 2006), although COL but not BFA also blocked the flow-induced [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    transient. We thus speculate that BK channel-mediated, flow-stimulated J\n                    <jats:sub>K<\/jats:sub>\n                    requires an increase in [Ca\n                    <jats:sup>2+<\/jats:sup>\n                    ]\n                    <jats:sub>i<\/jats:sub>\n                    due, in part, to luminal Ca\n                    <jats:sup>2+<\/jats:sup>\n                    entry and ER Ca\n                    <jats:sup>2+<\/jats:sup>\n                    release, microtubule integrity, and exocytic insertion of preformed channels into the apical membrane.\n                  <\/jats:p>","DOI":"10.1152\/ajprenal.00057.2007","type":"journal-article","created":{"date-parts":[[2007,3,27]],"date-time":"2007-03-27T23:53:28Z","timestamp":1175039608000},"page":"F227-F235","source":"Crossref","is-referenced-by-count":98,"title":["Ca\n                    <sup>2+<\/sup>\n                    dependence of flow-stimulated K secretion in the mammalian cortical collecting 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