Regulation of Ba2+-Induced Contraction of Murine Ureteral Smooth Muscle.
- Author:
Young Chul KIM
1
;
Moo Yeol LEE
;
Wun Jae KIM
;
Soon Chul MYUNG
;
Woong CHOI
;
Chan Hyung KIM
;
Wen Xie XU
;
Seung Ryul KIM
;
Sang Jin LEE
Author Information
1. Department of Physiology, Chungbuk National University College of Medicine, Cheongju 361-804, Korea. physiokyc@chungbuk.ac.kr
- Publication Type:Original Article
- Keywords:
Ureter;
Murine smooth muscle;
Ba2+;
Isoproterenol (ISO);
Cyclopiazonic acid (CPA)
- MeSH:
Adenylyl Cyclases;
Adrenergic beta-Agonists;
Ammonium Chloride;
Colforsin;
Glyburide;
Histamine;
Isoproterenol;
Membranes;
Mitochondria;
Muscle, Smooth*;
Neuropeptides;
Neurotransmitter Agents;
Nicardipine;
Potassium Channels, Calcium-Activated;
Potassium Channels, Inwardly Rectifying;
Quinidine;
Serotonin;
Ureter*
- From:The Korean Journal of Physiology and Pharmacology
2007;11(5):207-213
- CountryRepublic of Korea
- Language:English
-
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+/-0.06 mN (n=19). Neuropeptide and neurotransmitters such as serotonin (5microM), histamine (20microM), and carbarchol (CCh, 10~50microM) did not produce significant contraction. However, CCh (50microM) produced slow phasic contraction in the presence of 25 mM K+. Cyclopiazonic acid (CPA, 10microM), SR Ca2+-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 (10microM) and quinidine (20 microM) which are known to block Ca2+-activated K+ channels (KCa channel), ATP-sensitive K+ channels (KATP) and nonselective K+ channel, respectively, did not elicit any significant effect. However, Ba2+ (1~2 mM), blocker of inward rectifier K+ channels (KIR channel), produced phasic contraction in a reversible manner, which was blocked by 1microM nicardipine, a blocker of dehydropyridine-sensitive voltage-dependent L-type Ca2+ channels (VDCCL) in smooth muscle membrane. This Ba2+-induced phasic contraction was significantly enhanced by 10microM cyclopiazonic acid (CPA) in the frequency and amplitude. Finally, regulation of Ba2+-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 Ba2+-induced contraction (p<0.05). These results suggest that Ba2+ produces phasic contraction in murine ureteral smooth muscle which can be regulated by FSK and beta-adrenergic stimulation.
