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This Article Full Text Full Text (PDF) All Versions of this Article: 581/2/757    most recent jphysiol.2007.129536v1 Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via Google Scholar Google Scholar Articles by Tan, J. H. Articles by Brock, J. A. Search for Related Content PubMed PubMed Citation Articles by Tan, J. H. Articles by Brock, J. A. Related Collections Cardiovascular

¹ Prince of Wales Medical Research Institute, University of New South Wales, Barker Street, Randwick, NSW 2031, Australia

In rat tail artery, activation of postjunctional ₂-adrenoceptors by noradrenaline (NA) released from sympathetic axons produces a slow depolarization (NAD) of the smooth muscle through a decrease in K⁺ conductance. In this study we used intracellular recording to investigate whether the K⁺ channel involved is the ATP-sensitive K⁺ (K_ATP) channel. Changes in membrane resistance were monitored by measuring the time constant of decay of excitatory junction potentials. The K_ATP channel blockers, glibenclamide (10 µM) and PNU 37883A (5 µM), depolarized the smooth muscle and increased membrane resistance. Conversely, the K_ATP channel openers, pinacidil (0.1 and 0.5 µM) and levcromakalim (0.1 µM), hyperpolarized the smooth muscle and decreased membrane resistance. Activation of K_ATP channels with calcitonin gene-related peptide (CGRP; 10 nM) 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_ATP channel openers, pinacidil and levcromakalim, inhibited the NAD. The effects of other K⁺ channel blockers were also determined. A high concentration of Ba²⁺(1 mM), which would be expected to block K_ATP channels, abolished the NAD, whereas teteraethylammonium (1 mM) and 4-aminopyridine (1 mM) increased its amplitude. Apamin (0.5 µM) and a lower concentration of Ba²⁺ (0.1 mM) did not affect the NAD. These findings indicate that activation of ₂-adrenoceptors by neurally released NA depolarizes the membrane of vascular smooth muscle by inhibiting K_ATP channels open in the resting membrane.

(Received 30 January 2007; accepted after revision 19 March 2007; first published online 22 March 2007)
Corresponding author J. Brock: Prince of Wales Medical Research Institute, Barker St, Randwick, NSW 2031, Australia. Email: j.brock{at}unsw.edu.au