{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,6,24]],"date-time":"2026-06-24T06:55:59Z","timestamp":1782284159312,"version":"3.54.5"},"reference-count":33,"publisher":"American Physiological Society","issue":"1","content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["American Journal of Physiology-Heart and Circulatory Physiology"],"published-print":{"date-parts":[[2003,7]]},"abstract":"<jats:p>Steady shear stress stimulates transient hyperpolarization coupled to calcium-sensitive potassium (K<jats:sub>Ca<\/jats:sub>) channels and sustained depolarization linked to chloride-selective channels. Physiological flow is pulsatile not static, and whereas in vivo data suggest phasic shear stress may preferentially activate K<jats:sub>Ca<\/jats:sub>channels, its differential effects on both currents remain largely unknown. To determine this interaction, coronary endothelial cells were cultured in glass capillary flow tubes, loaded with the voltage-sensitive dye bis-(1,3-dibutylbarbituric acid)trimethine oxonol, and exposed to constant or pulsatile shear stress. The latter was generated by a custom servoperfusion system employing physiological pressure and flow waveforms. Steady shear induced a sustained depolarization inhibited by the Cl<jats:sup>-<\/jats:sup>channel blocker DIDS. Even after exposure to steady flow, subsequent transition to pulsatile shear stress further stimulated DIDS-sensitive depolarization. DIDS pretreatment \u201cunmasked\u201d a pulsatile flow-induced hyperpolarization of which magnitude was further enhanced by nifedipine, which augments epoxygenase synthesis. Pulse-shear hyperpolarization was fully blocked by K<jats:sub>Ca<\/jats:sub>channel inhibition (charybdotoxin + apamin), although these agents had no influence on membrane potential altered by steady flow. Thus K<jats:sub>Ca<\/jats:sub>-dependent hyperpolarization is preferentially stimulated by pulsatile over steady flow, whereas both can stimulate Cl<jats:sup>-<\/jats:sup>-dependent depolarization. This supports studies showing greater potency of pulsatile flow for triggering K<jats:sub>Ca<\/jats:sub>-dependent vasorelaxation.<\/jats:p>","DOI":"10.1152\/ajpheart.01072.2002","type":"journal-article","created":{"date-parts":[[2015,3,3]],"date-time":"2015-03-03T20:10:42Z","timestamp":1425413442000},"page":"H341-H346","source":"Crossref","is-referenced-by-count":13,"title":["Differential effects of pulsatile versus steady flow on coronary endothelial membrane potential"],"prefix":"10.1152","volume":"285","author":[{"given":"Wei-Ping","family":"Qiu","sequence":"first","affiliation":[{"name":"Division of Cardiology, Department of Medicine and Department of Biomedical Engineering, Johns Hopkins University, Baltimore, Maryland 21287"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Qinghua","family":"Hu","sequence":"additional","affiliation":[{"name":"Division of Cardiology, Department of Medicine and Department of Biomedical Engineering, Johns Hopkins University, 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