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Articles in PresS, published online ahead of print December 13, 2001
Am J Physiol Heart Circ Physiol, 10.1152/ajpheart.00837.2001
Submitted on September 25, 2001
Accepted on December 1, 2001
1 Neurosurgery, University of Mississippi Medical Center, Jackson, MS, USA
* To whom correspondence should be addressed. E-mail: jzhang{at}neurosurgery.umsmed.edu.
Chloride (Cl-) efflux induces depolarization and contraction of smooth muscle cells. This study was undertaken to explore the role of Cl- flux in histamine-induced contraction in the rabbit basilar artery. Male New Zealand white rabbits (n=16) weighting 1.8-2.5 kg were sacrificed by overdose of Phenobarbital. The basilar arteries were removed for isometric tension recording. Histamine produced a concentration-dependent contraction which was attenuated by H1receptor antagonist-chlorpheniramine (10 -8 M), but not by H2 receptor antagonist-cimetidine (3x10 -6M) in the normal Cl-Kreb's-Henseleit bicarbonate solution (123 mM Cl-). The histamine-induced contraction was reduced by the following manipulations: (a) Inhibition of Na+-K+-2Cl-cotransporter with bumetanide (3x10-5 and 10-4M). (b) Bicarbonate free HEPES solution to disable Cl-/HCO3- exchanger. (c) Blockade of Cl- channels using niflumic acid, 5-nitro-2-(3-phenylpropylamino) benzoic acid (NPPB), and indanyloxyacetic acid 94, R- (+)-methylindazone (R- (+)-IAA-94). In addition, substitution of extracellular Cl- with methanesulfonate acid (MS- 113 mM, Cl- 10 mM) transiently enhanced histamine-induced contraction. Manipulation of Cl- flux affects histamine-induced contraction in the rabbit basilar artery.
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