|
|
||||||||
Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, Nagoya City University, Japan.
1. Ionic currents underlying the action potential were recorded from enzymatically isolated smooth muscle cells of guinea-pig ureter. 2. The action potential recorded from a single cell was similar to that from a multicellular preparation. It showed repetitive spikes on a plateau potential which followed the first spike. Treatment with 10 mM-tetraethylammonium (TEA) increased the amplitude and duration of the plateau phase and abolished the repetitive spikes. 3. Under voltage clamp mode, at least two (maybe three) kinds of outward currents were activated during depolarizing pulses. The main outward current was Ca2+-dependent K+ current (IK(Ca], which was mostly blocked in Ca2+-free solution, or by application of 1 mM-cadmium (Cd2+) or 2 mM-tetraethylammonium (TEA). IK(Ca) was greatly decreased by treatment with 5 mM-caffeine or an addition of 10 mM-EGTA in a pipette solution. 4. In the presence of 1 mM-Cd2+ and 2 mM-TEA, a small transient outward current remained. 4-Aminopyridine (1 mM) suppressed the transient outward current by about 40%. Time- and voltage-dependent delayed rectifier outward currents were small in ureter cells. An inwardly rectifying K+ current was not detected. 5. An application of 1 mM-Cd2+, 5 mM-cobalt (Co2+), 1 mM-lanthanum (La3+) or 0.1 microM-nifedipine completely blocked the action potential. Replacement of 80-90% of extracellular Na+ with Li+ or Tris almost abolished the plateau potential and repetitive spikes but did not change significantly the first spike. 6. In the presence of 30 mM-TEA, the inward current elicited by depolarization was monophasic and lasted for more than 1 s. Application of 1 mM-Cd2+, 1 mM-La3+, 0.1 microM-nifedipine, or 5 mM-Co2+ completely blocked inward current. The replacement (87%) of extracellular Na+ ions with Li+, Tris, sucrose or TEA speeded up the decay of inward current; the inward current decreased by 10-60% at the end of a 500 ms pulse. 7. Even in low-Na+ solution (120 mM-TEA), the inactivation of ICa had a quite slow component (tau = 1 s), in addition to another faster component (tau = 100 ms) at 0 mV. When short depolarizing clamp pulses (50 ms) were repetitively applied at short intervals (50 ms) and with interpulse voltage of -10 or -20 mV to mimic the repetitive spikes on the plateau of the action potential, the decline of peak Ca2+ current during the train of pulses was smaller than the decay of Ca2+ current during a long pulse.(ABSTRACT TRUNCATED AT 400 WORDS)
This article has been cited by other articles:
![]() |
S. Hotta, K. Morimura, S. Ohya, K. Muraki, H. Takeshima, and Y. Imaizumi Ryanodine receptor type 2 deficiency changes excitation-contraction coupling and membrane potential in urinary bladder smooth muscle J. Physiol., July 15, 2007; 582(2): 489 - 506. [Abstract] [Full Text] [PDF] |
||||
![]() |
D. Yamazaki, M. Aoyama, S. Ohya, K. Muraki, K. Asai, and Y. Imaizumi Novel Functions of Small Conductance Ca2+-activated K+ Channel in Enhanced Cell Proliferation by ATP in Brain Endothelial Cells J. Biol. Chem., December 15, 2006; 281(50): 38430 - 38439. [Abstract] [Full Text] [PDF] |
||||
![]() |
R. J. Lang, M. A. Tonta, B. Z. Zoltkowski, W. F. Meeker, I. Wendt, and H. C. Parkington Pyeloureteric peristalsis: role of atypical smooth muscle cells and interstitial cells of Cajal-like cells as pacemakers J. Physiol., November 1, 2006; 576(3): 695 - 705. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Morimura, Y. Ohi, H. Yamamura, S. Ohya, K. Muraki, and Y. Imaizumi Two-step Ca2+ intracellular release underlies excitation-contraction coupling in mouse urinary bladder myocytes Am J Physiol Cell Physiol, February 1, 2006; 290(2): C388 - C403. [Abstract] [Full Text] [PDF] |
||||
![]() |
K. Sakamoto, T. Nonomura, S. Ohya, K. Muraki, T. Ohwada, and Y. Imaizumi Molecular Mechanisms for Large Conductance Ca2+-Activated K+ Channel Activation by a Novel Opener, 12,14-Dichlorodehydroabietic Acid J. Pharmacol. Exp. Ther., January 1, 2006; 316(1): 144 - 153. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Sade, K. Muraki, S. Ohya, N. Hatano, and Y. Imaizumi Activation of large-conductance, Ca2+-activated K+ channels by cannabinoids Am J Physiol Cell Physiol, January 1, 2006; 290(1): C77 - C86. [Abstract] [Full Text] [PDF] |
||||
![]() |
Y.-X. Wang, Y.-M. Zheng, Q.-B. Mei, Q.-S. Wang, M. L. Collier, S. Fleischer, H.-B. Xin, and M. I. Kotlikoff FKBP12.6 and cADPR regulation of Ca2+ release in smooth muscle cells Am J Physiol Cell Physiol, March 1, 2004; 286(3): C538 - C546. [Abstract] [Full Text] |
||||
![]() |
G. C. Amberg, S. D. Koh, Y. Imaizumi, S. Ohya, and K. M. Sanders A-type potassium currents in smooth muscle Am J Physiol Cell Physiol, March 1, 2003; 284(3): C583 - C595. [Abstract] [Full Text] [PDF] |
||||
![]() |
J. H. Jaggar, V. A. Porter, W. J. Lederer, and M. T. Nelson Calcium sparks in smooth muscle Am J Physiol Cell Physiol, February 1, 2000; 278(2): C235 - C256. [Abstract] [Full Text] [PDF] |
||||
![]() |
H. Yamamura, N. Nagano, M. Hirano, K. Muraki, M. Watanabe, and Y. Imaizumi Activation of Ca2+-Dependent K+ Current by Nordihydroguaiaretic Acid in Porcine Coronary Arterial Smooth Muscle Cells J. Pharmacol. Exp. Ther., October 1, 1999; 291(1): 140 - 146. [Abstract] [Full Text] |
||||
![]() |
P. Santicioli and C. A. Maggi Myogenic and Neurogenic Factors in the Control of Pyeloureteral Motility and Ureteral Peristalsis Pharmacol. Rev., December 1, 1998; 50(4): 683 - 722. [Abstract] [Full Text] [PDF] |
||||
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |