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BOTH EXTRACELLULAR ATP AND SHEAR STRESS REGULATE THE RELEASE OF NITRIC OXIDE IN RAT CAUDAL ARTERY
Author(s) -
Kwon Young Mi,
Shinozuka Kazumasa,
Kagota Satomi,
Yamaguchi Yu,
Nakamura Kazuki,
Kunitomo Masaru
Publication year - 1999
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1046/j.1440-1681.1999.03062.x
Subject(s) - extracellular , nitric oxide , perfusion , endogeny , medicine , contraction (grammar) , nitric oxide synthase , endocrinology , artery , chemistry , biophysics , biology , biochemistry
1. To elucidate the physiological role of nitric oxide (NO) in regulating vascular tone, the effects of N G ‐nitro‐ L ‐arginine methyl ester ( L ‐NAME), an NO synthase inhibitor, on the vasoconstrictor response to noradrenaline (NA) in rat caudal artery was examined. 2. N G ‐Nitro‐ L ‐arginine methyl ester significantly potentiated the NA‐induced increase in perfusion pressure in the perfused caudal artery, but did not affect the NA‐induced contraction in caudal artery ring preparations. In addition, an increase in perfusion pressure mechanically produced by a stepwise increase in flow rate was not affected by L ‐NAME. 3. Noradrenaline evoked a significant increase in the release of endogenous ATP and its metabolites from the perfused artery, whereas increased perfusion pressure as a result of increased flow rate did not evoke release of endogenous ATP. 4. In the presence of exogenously applied ATP, L ‐NAME significantly potentiated the increase in perfusion pressure produced by increased flow rate. 5. These results indicate that perfused vascular tone is regulated by endogenous NO and suggest that extracellular ATP may participate in the synthesis and release of NO by shear stress in endothelial cells in the rat caudal artery.