Regulation of $Ba^{2+}$-Induced Contraction of Murine Ureteral Smooth Muscle

  • Kim, Young-Chul (Departments of Physiology, Chungbuk National University College of Medicine) ;
  • Lee, Moo-Yeol (Departments of Physiology, College of Medicine Chung-Ang University) ;
  • Kim, Wun-Jae (Departments of Urology, Chungbuk National University College of Medicine) ;
  • Myung, Soon-Chul (Departments of Urology, College of Medicine Chung-Ang University) ;
  • Choi, Woong (Departments of Pharmacology, Chungbuk National University College of Medicine) ;
  • Kim, Chan-Hyung (Departments of Pharmacology, Chungbuk National University College of Medicine) ;
  • Xu, Wen-Xie (Departments of Physiology, College of Medicine, Shanghai Jiaotong University) ;
  • Kim, Seung-Ryul (Department of Biochemistry, Chungbuk National University College of Medicine) ;
  • Lee, Sang-Jin (Departments of Physiology, Chungbuk National University College of Medicine)
  • Published : 2007.10.31

Abstract

This study was designed to characterize ureteral smooth muscle motility and also to study the effect of forskolin(FSK) and isoproterenol(ISO) on smooth muscle contractility in murine ureter. High $K^+$(50 mM) produced tonic contraction by $0.17{\pm}0.06mN$(n=19). Neuropeptide and neurotransmitters such as serotonin($5{\mu}M$), histamine($20{\mu}M$), and carbarchol(CCh, $10{\sim}50{\mu}M$) did not produce significant contraction. However, CCh($50{\mu}M$) produced slow phasic contraction in the presence of 25 mM $K^+$. Cyclopiazonic acid(CPA, $10{\mu}M$), SR $Ca^{2+}$-ATPase blocker, produced tonic contraction(0.07 mN). Meanwhile, inhibition of mitochondria by protonophore carbnylcyanide m-chlorophenylhydrazone(CCCP) also produced weak tonic contraction(0.01 mN). The possible involvement of $K^+$ channels was also pursued. Tetraethyl ammonium chloride(TEA, 10 mM), glibenclamide($10{\mu}M$) and quinidine($20{\mu}M$) which are known to block $Ca^{2+}$-activated $K^+$ channels($K_{Ca}$ channel), ATP-sensitive $K^+$ channels($K_{ATP}$) and nonselective $K^+$ channel, respectively, did not elicit any significant effect. However, $Ba^{2+}$($1{\sim}2mM$), blocker of inward rectifier $K^+$ channels($K_{IR}$ channel), produced phasic contraction in a reversible manner, which was blocked by $1{\mu}M$ nicardipine, a blocker of dehydropyridine-sensitive voltage-dependent L-type $Ca^{2+}$ channels($VDCC_L$) in smooth muscle membrane. This $Ba^{2+}$-induced phasic contraction was significantly enhanced by $10{\mu}M$ cyclopiazonic acid(CPA) in the frequency and amplitude. Finally, regulation of $Ba^{2+}$-induced contraction was studied by FSK and ISO which are known as adenylyl cyclase activator and $\beta$-adrenergic receptor agonist, respectively. These drugs significantly suppressed the frequency and amplitude of $Ba^{2+}$-induced contraction(p<0.05). These results suggest that $Ba^{2+}$ produces phasic contraction in murine ureteral smooth muscle which can be regulated by FSK and $\beta$-adrenergic stimulation.

Keywords

References

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