Abstract:
:Nitric oxide formation by GH3 pituitary cells is stimulated by depolarizing concentrations of K+ and by the L-channel Ca2+ agonist Bay kappa 8644 in an additive manner that depends on extracellular Ca2+. Ca(2+)-dependent NO formation at 100 microM arginine was inhibited 50% over a 30-min period by 5 microM NG-amino-L-arginine, 30 microM N6-iminoethyl-L-ornithine (NIO) and 520 microM N5-iminoethyl-L-lysine (NIL) but required concentrations of aminoguanidine (AG) greater than 3 mM. As measured at 100 microM extracellular arginine, intracellular neuronal nitric oxide synthase (nNOS) was inactivated 50% over a 30-min period by 150 microM NG-amino-L-arginine and 1500 microM NIO, but required concentrations of NIL or AG greater than 5 mM. The inactivation of nNOS by these agents occurred only under conditions that mobilized extracellular Ca2+ and was inhibited by increased extracellular arginine. Thus these agents inhibit cellular Ca(2+)-dependent NO formation at concentrations far lower than those required to inactivate the cellular nNOS. Inhibition of NO formation by these agents was not attributable to effects on cellular arginine uptake. In contrast diphenyliodonium chloride produced a rapid and complete inactivation of cellular NO formation and nNOS activity. These inactivations produced by diphenyliodonium chloride occurred with identical kinetics but displayed no requirement for Ca2+. These data support the assertion that neuronal NO synthase is refractory to mechanism-based inactivation in GH3 pituitary cells.
journal_name
Arch Biochem Biophysjournal_title
Archives of biochemistry and biophysicsauthors
Cooper GR,Barr A,Wolff DJdoi
10.1006/abbi.1998.0828subject
Has Abstractpub_date
1998-09-15 00:00:00pages
195-206issue
2eissn
0003-9861issn
1096-0384pii
S0003-9861(98)90828-1journal_volume
357pub_type
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journal_title:Archives of biochemistry and biophysics
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pub_type: 杂志文章
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pub_type: 杂志文章
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更新日期:2002-01-15 00:00:00
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pub_type: 杂志文章
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更新日期:1998-10-01 00:00:00