| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
|
|
|
|||||||
|
|||||||||
Institute of Biomedical and Life Sciences, University of Glasgow, UK.
1. Ca2+ current through voltage-dependent Ca2+ channels (ICa) and intracellular free Ca2+ concentration ([Ca2+]i) were measured simultaneously in rat portal vein smooth muscle cells using conventional whole-cell voltage clamp technique and high temporal resolution microfluorimetry. 2. The relationship between depolarization-evoked ICa and rise in [Ca2+]i was examined. The extracellular Ca2+ concentration dependence and the voltage dependence of the depolarization-evoked increases in ICa and [Ca2+]i were similar. Both ICa and increased [Ca2+]i were blocked to a similar extent by nimodipine and cadmium and augmented by Bay K 8644. Furthermore, the time course of the measured increase in [Ca2+]i, closely followed the increase in [Ca2+]i expected from the time-integrated ICa. These observations suggest that the depolarization-evoked rise in [Ca2+]i was tightly coupled to ICa. 3. The cytosolic Ca2+ buffering capacity, determined as the ratio of the expected increase in [Ca2+]i (from ICa) divided by the measured increase in [Ca2+]i, was over 100. Therefore, less than 1 out of 100 Ca2+ ions entering the cell appears as a free Ca2+. 4. Ryanodine (30 microM), a blocker of the Ca(2+)-induced Ca2+ release mechanism, had little effect on buffering capacity measured over the first 200 ms of the depolarizing voltage clamp pulse. Ryanodine also had little effect on the buffering capacity during 800-1000 ms of the depolarizing voltage clamp pulse. Therefore, it was concluded that there is little Ca(2+)-induced Ca2+ release from the stores in rat portal vein smooth muscle cells during depolarization-evoked Ca2+ entry. 5. During brief depolarizations, the largest [Ca2+]i increase and ICa occurred at 0 mV. However, during steady-state depolarization, the largest increase in [Ca2+]i occurred around -30 mV, and we estimate the peak steady-state ICa to be about 0.6 pA.
This article has been cited by other articles:
|
|
 |
|
  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]
|
|
|
|
|
|
S. N. Saleh and I. A. Greenwood Activation of chloride currents in murine portal vein smooth muscle cells by membrane depolarization involves intracellular calcium release Am J Physiol Cell Physiol, January 1, 2005; 288(1): C122 - C131. [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]
|
|
|
|
 |
|
 T. Kamishima and J. M. Quayle P2 receptor-mediated Ca2+ transients in rat cerebral artery smooth muscle cells Am J Physiol Heart Circ Physiol, February 1, 2004; 286(2): H535 - H544. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
R. P. Burt Phasic contractions of the rat portal vein depend on intracellular Ca2+ release stimulated by depolarization Am J Physiol Heart Circ Physiol, May 1, 2003; 284(5): H1808 - H1817. [Abstract] [Full Text] [PDF]
|
|
|
|
|
|
T. Kamishima and J. M. Quayle Mitochondrial Ca2+ uptake is important over low [Ca2+]i range in arterial smooth muscle Am J Physiol Heart Circ Physiol, December 1, 2002; 283(6): H2431 - H2439. [Abstract] [Full Text] [PDF]
|
|
|
|
 |
|
 G.L. Smith, C. Austin, C. Crichton, and S. Wray A review of the actions and control of intracellular pH in vascular smooth muscle Cardiovasc Res, May 1, 1998; 38(2): 316 - 331. [Abstract] [Full Text] [PDF]
|
|
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH | TABLE OF CONTENTS |
