Am J Physiol Cell Physiol Watch the video to learn how APS reaches out to developing nations.
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

Am J Physiol Cell Physiol 262: C691-C700, 1992;
0363-6143/92 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Vogalis, F.
Right arrow Articles by Sanders, K. M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Vogalis, F.
Right arrow Articles by Sanders, K. M.

AJP - Cell Physiology, Vol 262, Issue 3 C691-C700, Copyright © 1992 by American Physiological Society

ARTICLES

Regulation of calcium current by voltage and cytoplasmic calcium in canine gastric smooth muscle

F. Vogalis, N. G. Publicover and K. M. Sanders
Department of Physiology, University of Nevada School of Medicine, Reno 89557.

The regulation of Ca2+ current by intracellular Ca2+ was studied in isolated myocytes from the circular layer of canine gastric antrum. Ca2+ current was measured with the whole cell patch-clamp technique, and changes in cytoplasmic Ca2+ ([Ca2+]i) were simultaneously measured with indo-1 fluorescence. Ca2+ currents were activated by depolarization and inactivated despite maintained depolarization. Ca2+ current inactivation was fit with a double exponential function. Using Ba2+ or Na+ as charge carriers removed the fast component of inactivation, whereas enhanced intracellular buffering of Ca2+ did not remove the fast component. Ca2+ currents were associated with a rise in [Ca2+]i. The decrease in [Ca2+]i following repolarization was exponential, and during the relaxation of [Ca2+]i, Ca2+ current was inactivated. The inward current recovered with a similar time course as the decrease in [Ca2+]i, suggesting that [Ca2+]i regulates the basal availability of Ca2+ channels. These data support the hypothesis that, although [Ca2+]i may influence the resting level of inactivation, it is the "submembrane" compartment of [Ca2+]i that regulates the development of inactivation.


This article has been cited by other articles:


Home page
 Am. J. Physiol. Gastrointest. Liver Physiol.Home page
A. Muinuddin, Y. Kang, H. Y. Gaisano, and N. E. Diamant
Regional differences in L-type Ca2+ channel expression in feline lower esophageal sphincter
Am J Physiol Gastrointest Liver Physiol, October 1, 2004; 287(4): G772 - G781.
[Abstract] [Full Text] [PDF]

Home page
 J. Appl. Physiol.Home page
K. M. Sanders
Signal Transduction in Smooth Muscle: Invited Review: Mechanisms of calcium handling in smooth muscles
J Appl Physiol, September 1, 2001; 91(3): 1438 - 1449.
[Abstract] [Full Text] [PDF]

Home page
 Physiol. Rev.Home page
H. KURIYAMA, K. KITAMURA, T. ITOH, and R. INOUE
Physiological Features of Visceral Smooth Muscle Cells, With Special Reference to Receptors and Ion Channels
Physiol Rev, July 1, 1998; 78(3): 811 - 920.
[Abstract] [Full Text] [PDF]

Home page
 Pharmacol. Rev.Home page
H. Karaki, H. Ozaki, M. Hori, M. Mitsui-Saito, K.-I. Amano, K.-I. Harada, S. Miyamoto, H. Nakazawa, K.-J. Won, and K. Sato
Calcium Movements, Distribution, and Functions in Smooth Muscle
Pharmacol. Rev., June 1, 1997; 49(2): 157 - 230.
[Abstract] [Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online