ArticleThe Journal of membrane biology1987
Involvement of calcium in calcium-current inactivation in smooth muscle cells from rat vas deferens.
Article in The Journal of membrane biology, 1987. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
3 citing papers in PubMed.
- Effects of nifedipine and ryanodine on adrenergic neurogenic contractions of rat vas deferens: evidence for a pulse-to-pulse change in Ca2+ sources.British journal of pharmacology · 1993Article
- Effects of calcitonin gene-related peptide (CGRP) on Ca(2+)-channel current of isolated smooth muscle cells from rat vas deferens.Naunyn-Schmiedeberg's archives of pharmacology · 1992Article
- Endothelin activates the dihydropyridine-sensitive, voltage-dependent Ca2+ channel in vascular smooth muscle.Proceedings of the National Academy of Sciences of the United States of America · 1989Article
Corrections and comments
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Authors and funding
3 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Ca-channel currents were recorded in Cs-loaded single smooth muscle cells from rat vas deferens to define the dependence of the inactivation time course on Ca concentration. The decay of Ca-channel current obtained in a Ba2+- or Sr2+-containing external solution during long voltage-clamp pulses was much slower than that in a Ca-containing solution. The difference was not due to a change in the surface potential of the membrane as judged from the steady-state activation and inactivation curves. When Ca was the charge carrier, increasing external Ca concentration slightly accelerated the rate of inactivation. In addition, the rate of inactivation of Ca-channel current in 10.8 mM Ba was also accelerated by adding Ca to the external solution in a concentration-dependent manner. The time course of Ca-current inactivation was slowed when the cells were dialyzed with a high concentration of citrate, a Ca-chelating agent. From these results, we concluded that a mechanism regulated by intracellular Ca activity plays a role in the inactivation of Ca channels in smooth muscle. The Ca-dependent process may protect against Ca overload by regulating Ca entry in smooth muscle cells.
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Registered trials
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