The Korean Journal of Pharmacology (대한약리학회지)

The Korean Society of Pharmacology (대한약리학회)
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Acid Secretion and Nitric Oxide Synthase Activity in Gastric Glands Following Hypoxia/Reoxygenation and Acidosis

Hypoxia/Reoxygenation과 Acidosis가 위선세포에서 위산분비와 NO Synthase 활성에 미치는 영향

  • Kim Hye-Young (Department of Pharmacology, Yonsei University College of Medicine) ;
  • Kim Kyung-Hwan (Department of Pharmacology, Yonsei University College of Medicine)
  • 김혜영 (연세대학교 의과대학 약리학교실) ;
  • 김경환 (연세대학교 의과대학 약리학교실)
  • Published : 1995.06.01
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Abstract

Acid secretion and NO synthase activity were determined in isolated gastric glands following hypoxia/reoxygenation and acidosis to investigate the involvement of NO in acid secretion. Isolated gastric glands were exposed to hypoxia (30 min)/reoxygenation (1 h) and/or to acidosis (pH 6.0 and 4.0). Acid secretion was measured by the ratio of $[^{14}C]-aminopyrine$ accumulation between intra- and extraglands. NO synthase activity was determined by percent conversion to $[^{14}C]-citrulline\;from\;[^{14}C]L-arginine$, a precursor of NO. The results indicate that dibutyryl cAMP stimulated acid secretion dose-dependently but had no effect on NO synthase activity in basal gastric glands. Hypoxia/reoxygenation significantly suppressed acid secretion both in unstimulated and stimulated gastric glands, which was exaggerated by acidosis. Constitutive NO synthase, activity, not responded to dibutyryl cAMP, was also inhibited by hypoxia/reoxygenation and acidosis. In conclusion, pathologic state of gastric mucosa such as hypoxia/reoxygenation and acidosis suppresses both acid secretion and NO release but the role of NO in acid secretion stimulated by dibutyryl cAMP in basal gastric glands is not significant.

NO의 위산분비에 대한 작용을 규명하기 위하여 분리한 토끼위선세포에서 hypoxia/reoxygenation과 acidosis후 위산분비와 NO synthase 활성을 측정하였다. 분리한 위선세포에 30분의 hypoxia와 1시간의 reoxygenation을 주었으며, acidosis를 위하여 배지의 pH를 6.0과 4.0으로 변화시켜 실험하였다. 위산분비는 위선세포 내와 외의 $[^{14}C]-aminopyrine$ 축적비율로 측정하였으며, NO synthase 활성은 NO의 전구물질인 $[^{14}C]L-arginine$으로부터 $[^{14}C]-citrulline$으로의 전환율로 결정하였다. 결과로서 dibutyryl cAMP는 농도 의존적으로 위산분비를 촉진시켰으나 NO synthase 활성엔 영향을 주지 않았다. Hypoxia/reoxygenation은 기초 및 자극 위산분비를 억제하였으며 acidosis에 의해 위산분비억제는 더욱 심화되었다. Constitutive NO synthase 활성 역시 hypoxia/reoxygenation과 acidosis에 의해 억제되었다. 결론적으로 hypoxia/reoxygenation과 acidosis 같은 위점막의 병적상태는 위산분비와 NO 유리를 모두 억제하나, 기초상태의 위선에서 dibutyryl cAMP에 의한 위산분비 촉진에 대한 NO의 직접적인 작용은 확인되지 않았다.

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