토끼 기관평활근 수축에서 G Protein의 역할

Role of G-protein in the Contraction of Rabbit Trachealis Muscle

  • 정진섭 (부산대학교 의과대학 생리학교실) ;
  • 황태호 (부산대학교 치과대학 생리학교실) ;
  • 이상호 (부산대학교 의과대학 생리학교실)
  • Jung, Jin-Sup (Department of Physiology, Pusan University School of Medicine) ;
  • Hwang, Tae-Ho (Department of Physiology, Pusan University School of Dentistry) ;
  • Lee, Sang-Ho (Department of Physiology, Pusan University School of Medicine)
  • 발행 : 1990.12.30

초록

Fluoride (F-), a known stimulator of G-protein, induced strong contraction in rabbit trachealis muscle. $AlCl_3\;(5{\sim}20\;{\mu}M)$, which is required for G-protein stimulation by $F^-$, potentiated the contractile response to $F^-$. $Ca^{2+}-removal$ and verapamil, a calcium channel blocker, inhibited the fluoroaluminate-induced contraction. Fluoroaluminate increased $^{45}Ca$ influx in the absence and presence of verapamil. In heparin-loaded muscle high $K^+-induced$ contraction was not affected, but acetylcholine and fluoroaluminate-induced contractions were inhibited. The fluoroaluminate-induced contraction was partially relaxed by isoproterenol, a stimulator of adenylate cyclase. Pertussis toxin partially inhibited fluoroaluminate-induced contraction and potentiated isoproterenol-induced relaxation in the presence of fluoroaluminate, but had no effect on acetylcholine-induced contraction and the isoproterenol-induced relaxation in the presence of acetylcholine. These results suggest that fluoroaluminate has the ability to stimulate at least two putative G-proteins in rabbit trachealis muscle; One causes $Ca^{2+}$ influx through the potential-operated $Ca^{2+}$ channel and the other induces intracellular $Ca^{2+}$ release by the increase of inositol-1, 4, 5-triphosphate.

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