{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2025,10,27]],"date-time":"2025-10-27T15:54:46Z","timestamp":1761580486731,"version":"3.33.0"},"reference-count":32,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2007,5,23]],"date-time":"2007-05-23T00:00:00Z","timestamp":1179878400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["The Journal of Physiology"],"published-print":{"date-parts":[[2007,6]]},"abstract":"<jats:p>In rat tail artery, activation of postjunctional \u03b1<jats:sub>2<\/jats:sub>\u2010adrenoceptors by noradrenaline (NA) released from sympathetic axons produces a slow depolarization (NAD) of the smooth muscle through a decrease in K<jats:sup>+<\/jats:sup>conductance. In this study we used intracellular recording to investigate whether the K<jats:sup>+<\/jats:sup>channel involved is the ATP\u2010sensitive K<jats:sup>+<\/jats:sup>(K<jats:sub>ATP<\/jats:sub>) channel. Changes in membrane resistance were monitored by measuring the time constant of decay of excitatory junction potentials. The K<jats:sub>ATP<\/jats:sub>channel blockers, glibenclamide (10 \u03bc<jats:sc>m<\/jats:sc>) and PNU 37883A (5 \u03bc<jats:sc>m<\/jats:sc>), depolarized the smooth muscle and increased membrane resistance. Conversely, the K<jats:sub>ATP<\/jats:sub>channel openers, pinacidil (0.1 and 0.5 \u03bc<jats:sc>m<\/jats:sc>) and levcromakalim (0.1 \u03bc<jats:sc>m<\/jats:sc>), hyperpolarized the smooth muscle and decreased membrane resistance. Activation of K<jats:sub>ATP<\/jats:sub>channels with calcitonin gene\u2010related peptide (CGRP; 10 n<jats:sc>m<\/jats:sc>) also hyperpolarized the smooth muscle and decreased membrane resistance. The NAD was abolished by both glibenclamide and PNU 37883A but was potentiated by CGRP. However, unlike CGRP, the directly acting K<jats:sub>ATP<\/jats:sub>channel openers, pinacidil and levcromakalim, inhibited the NAD. The effects of other K<jats:sup>+<\/jats:sup>channel blockers were also determined. A high concentration of Ba<jats:sup>2+<\/jats:sup>(1 m<jats:sc>m<\/jats:sc>), which would be expected to block K<jats:sub>ATP<\/jats:sub>channels, abolished the NAD, whereas teteraethylammonium (1 m<jats:sc>m<\/jats:sc>) and 4\u2010aminopyridine (1 m<jats:sc>m<\/jats:sc>) increased its amplitude. Apamin (0.5 \u03bc<jats:sc>m<\/jats:sc>) and a lower concentration of Ba<jats:sup>2+<\/jats:sup>(0.1 m<jats:sc>m<\/jats:sc>) did not affect the NAD. These findings indicate that activation of \u03b1<jats:sub>2<\/jats:sub>\u2010adrenoceptors by neurally released NA depolarizes the membrane of vascular smooth muscle by inhibiting K<jats:sub>ATP<\/jats:sub>channels open in the resting membrane.<\/jats:p>","DOI":"10.1113\/jphysiol.2007.129536","type":"journal-article","created":{"date-parts":[[2007,3,23]],"date-time":"2007-03-23T00:08:22Z","timestamp":1174608502000},"page":"757-765","source":"Crossref","is-referenced-by-count":9,"title":["Inhibition of K<sub>ATP<\/sub>channels in the rat tail artery by neurally released noradrenaline acting on postjunctional \u03b1<sub>2<\/sub>\u2010adrenoceptors"],"prefix":"10.1113","volume":"581","author":[{"given":"Joy H.","family":"Tan","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Amr","family":"Al Abed","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"James 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