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Peroxynitrite hyperpolarizes smooth muscle and relaxes internal carotid artery in rabbit via ATP-sensitive K⁺ channels

¹Cardiovascular Center and Department of Internal Medicine and ²Pharmacology, The University of Iowa and Roy J. and Lucille A. Carver College of Medicine; and ³Veterans Affairs Medical Center, Iowa City, Iowa

Submitted 16 March 2005 ; accepted in final form 8 July 2005

The goal of this study was to determine the effects of peroxynitrite (ONOO^–) on smooth muscle membrane potential and vasomotor function in rabbit carotid arteries. ONOO^– is known to affect vascular tone by several mechanisms, including effects on K⁺ channels. Xanthine (X, 0.1 mM), xanthine oxidase (XO, 0.01 U/ml), and a low concentration of sodium nitroprusside (SNP, 10 nM) were used to generate ONOO^–. In the common carotid artery, X and XO (X/XO) in the presence of SNP tended to increase tension. In contrast, in the internal carotid artery, X/XO in the presence of SNP transiently hyperpolarized the membrane (–8.5 ± 1.8 mV, mean ± SE) and decreased tension (by 85 ± 5.6%). In internal carotid arteries, in the absence of SNP, X/XO did not hyperpolarize the membrane and produced much less relaxation (by 23 ± 5.6%) than X/XO and SNP. Ebselen (50 µM) inhibited both hyperpolarization and relaxation to X/XO and SNP, and uric acid (100 µM) inhibited relaxation. Glibenclamide (1 µM) abolished hyperpolarization and inhibited relaxation during X/XO and SNP. Charybdotoxin (100 nM) or tetraethylammonium (1 mM) did not affect hyperpolarization or relaxation, respectively. These results suggest that ONOO^– hyperpolarizes and relaxes smooth muscle in rabbit internal carotid artery but not in common carotid artery through activation of K_ATP channels.

hyperpolarization; membrane potential; vasomotor function; reactive oxygen species

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