{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2024,7,4]],"date-time":"2024-07-04T07:10:53Z","timestamp":1720077053228},"reference-count":26,"publisher":"Wiley","issue":"4","license":[{"start":{"date-parts":[[2009,2,11]],"date-time":"2009-02-11T00:00:00Z","timestamp":1234310400000},"content-version":"vor","delay-in-days":4151,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["bpspubs.onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["British J Pharmacology"],"published-print":{"date-parts":[[1997,10]]},"abstract":"<jats:p>\n<jats:list list-type=\"explicit-label\">\n<jats:list-item><jats:p>Double\u2010barrelled ion\u2010selective microelectrodes were used to examine the effects of exogenous noradrenaline upon the membrane potential (E<jats:sub>m<\/jats:sub>) and intracellular chloride concentration ([Cl]<jats:sub>i<\/jats:sub>) of arterial smooth muscle from the saphenous branch of the femoral artery of the rat.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>After treatment with 0.6\u2003m<jats:sc>M<\/jats:sc>\u20036\u2010hydroxydopamine (to functionally denervate the tissue), exogenous noradrenaline (5\u2003n<jats:sc>M<\/jats:sc>) caused repeatable depolarization of E<jats:sub>m<\/jats:sub> from \u221263.7\u00b12.4\u2003mV (s.d., <jats:italic>n<\/jats:italic>=18) to \u221253.8\u00b13.4\u2003mV (<jats:italic>P<\/jats:italic>&lt;0.0001) and increases in [Cl]<jats:sub>i<\/jats:sub> from 31.0\u00b10.5\u2003m<jats:sc>M<\/jats:sc> to 42.5\u00b12.2\u2003m<jats:sc>M<\/jats:sc> (<jats:italic>P<\/jats:italic>&lt;0.0001).<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In the presence of 10\u2003\u03bc<jats:sc>M<\/jats:sc> bumetanide (an inhibitor of (Na\u2010K\u2010Cl) cotransport), 5\u2003n<jats:sc>M<\/jats:sc> noradrenaline caused a depolarization of E<jats:sub>m<\/jats:sub> of 3.0\u00b13.2\u2003mV, and a rise in [Cl]<jats:sub>i<\/jats:sub> of 4.5\u00b12.5\u2003m<jats:sc>M<\/jats:sc>.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In the presence of bumetanide and 1\u2003m<jats:sc>M<\/jats:sc> acetazolamide (used as an inhibitor of a Na\u2010independent inward Cl pump), noradrenaline had no effect on E<jats:sub>m<\/jats:sub> or [Cl]<jats:sub>i<\/jats:sub>.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>In the absence of extracellular chloride, the rise in apparent [Cl]<jats:sub>i<\/jats:sub> in response to 5\u2003n<jats:sc>M<\/jats:sc> noradrenaline was abolished but there was a depolarization of 2.0\u00b13.9\u2003mV.<\/jats:p><\/jats:list-item>\n<jats:list-item><jats:p>These results are consistent with the stimulation of (Na\u2010K\u2010Cl) cotransport and a Na\u2010independent Cl pump by exogenous noradrenaline and with the consequent increase in [Cl]<jats:sub>i<\/jats:sub> and shift in E<jats:sub>Cl<\/jats:sub> potentiating the depolarization caused by noradrenaline. The possibility that modulation of [Cl]<jats:sub>i<\/jats:sub> may be a general mechanism of E<jats:sub>m<\/jats:sub> regulation is discussed.<\/jats:p><\/jats:list-item>\n<\/jats:list>\n<\/jats:p><jats:p><jats:italic>British Journal of Pharmacology<\/jats:italic> (1997) <jats:bold>122<\/jats:bold>, 639\u2013642; doi:<jats:ext-link xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" ext-link-type=\"doi\" xlink:href=\"10.1038\/sj.bjp.0701431\">10.1038\/sj.bjp.0701431<\/jats:ext-link><\/jats:p>","DOI":"10.1038\/sj.bjp.0701431","type":"journal-article","created":{"date-parts":[[2005,1,28]],"date-time":"2005-01-28T19:14:06Z","timestamp":1106939646000},"page":"639-642","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":18,"title":["Stimulation of intracellular chloride accumulation by noradrenaline and hence potentiation of its depolarization of rat arterial smooth muscle <i>in vitro<\/i>"],"prefix":"10.1111","volume":"122","author":[{"given":"Julian P. 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