The role of the sarcolemmal Ca(2+)-ATPase in the pH transients associated with contraction in rat smooth muscle
1. We have investigated the origin of the intracellular acid pH transients that accompany myometrial contraction. Intra- and extracellular pH were measured with SNARF and intracellular Ca2+ concentration ([Ca2+]i) with indo-1. 2. An intracellular acidification accompanied spontaneous contractions an...
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Published in: | The Journal of physiology Vol. 505; no. Pt 2; pp. 329 - 336 |
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Main Authors: | , , , , , |
Format: | Journal Article |
Language: | English |
Published: |
England
The Physiological Society
01-12-1997
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Subjects: | |
Online Access: | Get full text |
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Summary: | 1. We have investigated the origin of the intracellular acid pH transients that accompany myometrial contraction. Intra- and
extracellular pH were measured with SNARF and intracellular Ca2+ concentration ([Ca2+]i) with indo-1. 2. An intracellular
acidification accompanied spontaneous contractions and those elicited by KCl depolarization or the addition of the agonists
carbachol or prostaglandin F2 alpha. The size of the acidification increased with the magnitude of the contraction. 3. The
intracellular acidification was accompanied by an extracellular alkalinization, showing that it results from proton movement
across the surface membrane. Furthermore, it was decreased either by addition of Cd2+ (20 nM, an inhibitor of the sarcolemmal
Ca(2+)-ATPase) or by elevating [Ca2+]o. 4. Extracellular alkalinization increased the magnitude of the rise of [Ca2+]i and
force produced by KCl. 5. An intracellular acidification was also associated with contraction in the portal vein and ureter.
6. We conclude that the sarcolemmal Ca(2+)-ATPase produces a significant intracellular acidification while removing Ca2+.
Both the acidification and decrease of [Ca2+]i will promote relaxation. Since Ca2+ and protons have opposite effects on many
cellular processes, this dual regulation by these two ions may be of general importance. |
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Bibliography: | ObjectType-Article-1 SourceType-Scholarly Journals-1 ObjectType-Feature-2 content type line 23 |
ISSN: | 0022-3751 1469-7793 |
DOI: | 10.1111/j.1469-7793.1997.329bb.x |