| 17379634 |
Tan JH, Al Abed A, Brock JA: Inhibition of KATP channels in the rat tail artery by neurally released noradrenaline acting on postjunctional alpha2-adrenoceptors. J Physiol. 2007 Jun 1;581(Pt 2):757-65. Epub 2007 Mar 22.
In rat tail artery, activation of postjunctional alpha (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 microm) and PNU 37883A (5 microm), depolarized the smooth muscle and increased membrane resistance. Conversely, the K (ATP) channel openers, pinacidil (0.1 and 0.5 microm) and levcromakalim (0.1 microm), 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 Ba (2+)(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 microm) and a lower concentration of Ba (2+) (0.1 mM) did not affect the NAD. These findings indicate that activation of alpha (2)-adrenoceptors by neurally released NA depolarizes the membrane of vascular smooth muscle by inhibiting K (ATP) channels open in the resting membrane. |
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