Korean J Physiol Pharmacol.
2007 Oct;11(5):207-213.
Regulation of Ba2+-Induced Contraction of Murine Ureteral Smooth Muscle
- Affiliations
-
- 1Department of Physiology, Chungbuk National University College of Medicine, Cheongju 361-804, Korea. physiokyc@chungbuk.ac.kr
- 2Department of Urology, Chungbuk National University College of Medicine, Cheongju 361-804, Korea.
- 3Department of Pharmacology, Chungbuk National University College of Medicine, Cheongju 361-804, Korea.
- 4Department of Biochemistry, Chungbuk National University College of Medicine, Cheongju 361-804, Korea.
- 5Departments of 1Physiology, and 3Urology, College of Medicine, Chung-Ang University, Seoul 156-756, Korea.
- 6Department of Physiology, College of Medicine, Shanghai Jiaotong University, 800 Dongchun Rd. Shanghai, 200240, P.R. China.
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.
MeSH Terms
-
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*
Adrenergic beta-Agonists
Ammonium Chloride
Colforsin
Glyburide
Histamine
Isoproterenol
Neuropeptides
Neurotransmitter Agents
Nicardipine
Potassium Channels, Calcium-Activated
Potassium Channels, Inwardly Rectifying
Quinidine
Serotonin
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