EFFECTS OF HYDROGEN PEROXIDE ON STIMULATORY GUANINE NUCLEOTIDE-BINDING PROTEIN IN RAT HEART
スポンサーリンク
概要
- 論文の詳細を見る
This study was undertaken to examine the effects of hydrogen peroxide on stimulatory guanine nucleotide-binding protein (Gs), and coupling in the β-aderenergic receptor - Gs - adenylate cyclase system in rat heart, in vitro. Cardiac membranes were preincubated with various concentrations (0.1, 1 , and 10 mM) of hydrogen peroxide at 30℃ for 5, 10, 30 and 60 min. Although the assay of β-adrenergic receptors involving [^3H]-dihydroaloprenolol ([^3H]-DHA) binding revealed that the maximal number of binding sites (B_<max>) was not altered, the dissociation constant (K_d) for [^3H]-DHA was increased in the presence of I mM and 10 mM hydrogen peroxide (control 0.68±0.16 nM, vs 1 mM H202 1.13±0.16, 10 mM H202 1.01±0. 12). Conversely, no significant changes in Gs activities were observed in hydrogen peroxide-treated groups. Adenylate cyclase activity (stimulated by forskolin) was significantly reduced by 10 mM hydrogen peroxide after a 5 min preincubation period (control 277.1±19.2 pmol cAMP/mg protein/min, H202 230.3±14.9). The amounts of cyclic AMP produced by the stimulation of membranes with GTP, GTP + (1)-isoproterenol, guanylimidodiphosphate (Gpp(NH)p) or Gpp(NH)p+(1)-isoproterenol were significantly lower in 10 mM hydrogen peroxide-treated groups than those in controls (GTP: control 57.6±5.6pmol cAMP/mg protein/min vs H_2O_2 46.4±6.9, GTP+(1)-isoproterenol: control 83.9±10.2 vs H_2O_2 67.7±10.3, Gpp(NH)p: control 77.5±8.8 vs H_2O_2 61.0±8.6. Gpp(NH)p+(1)-isoproterenol: control 105.0±13.1 vs H202 83.9±12.2, forskolin: control 223.2±13.8 vs H202 182.8±18.4). In the presence of hydrogen peroxide, the extents of the depression in cAMP production induced by GTP. GTP+isoproterenol, Gpp(NH)p, and Gpp(NH)p+ (1)-isoproterenol were similar to those induced by forskolin stimulation. These results indicate that hydrogen peroxide does not affect Gs activity or coupling in the p-receptor - Gs - adenylate cyclase system, but does depress CAMP production by inhibiting adenylate cyclase.
- 社団法人日本循環器学会の論文
- 1993-09-20
著者
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Hayashi Hideharu
Photon Medical Research Center, Hamamatsu University School of Medicine
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Yamazaki Noboru
Third Department of Internal Medicine, Hamamatsu University School of Medicine
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Kaneko Masanori
Third Department of Internal Medicine, Hamamatsu University School of Medicine
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Kaneko Masanori
Third Department Of Internal Medicine Hamamatsu University School Of Medicine
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Kaneko Masanori
浜松医科大学 第3内科
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KOBAYASHI AKIRA
The Third Department of Internal Medicine, Hamamatsu University School of Medicine
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Kobayashi Akira
Third Department of Internal Medicine, Hamamatsu University School of Medicine
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Hayashi Hideharu
Photon Medical Research Center Hamamatsu University School Of Medicine
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Yamazaki Noboru
Third Division Department Of Internal Medicine Hamamatsu University School Of Medicine
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Yamazaki Noboru
The Third Department Of Internal Medicine Hamamatsu University School Of Medicine
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Kobayashi Akira
The Department Of Medicine Iii Hamamatsu University School Of Medicine
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MASUDA HISAMICHI
Third Department of Internal Medicine
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RONG BANG
Third Department of Internal Medicine
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IKEGAYA TAKAYOSHI
Third Department of Internal Medicine
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Kobayashi Akira
Internal Medicine Iii Hamamatsu University School Of Medicine
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Yamazaki Noboru
Third Department Of Internal Medicine Hamamatsu University School Of Medicine
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Kaneko Masanori
Department Of Cardiology Hamamatsu Medical Cente
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Yamazaki Noburu
The Third Department Of Internal Medicine Hamamatsu University School Of Medicine
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Yamazaki Noboru
The 2nd Dept. Of Intern Med. Nagoya Univ. School. Of Med.
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Yamazaki Noboru
Nanotechnology Research Institute National Institute Of Advanced Industrial Science And Technology (
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