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Modulation of aortic smooth muscle cell membrane potential by extracellular calcium.
Author(s) -
Carlos E. Palant,
Naftali Stern,
Alexander Meyer,
M L Tuck,
D B Lee,
Norimoto Yanagawa
Publication year - 1989
Publication title -
hypertension
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.986
H-Index - 265
eISSN - 1524-4563
pISSN - 0194-911X
DOI - 10.1161/01.hyp.14.5.549
Subject(s) - extracellular , calcium , depolarization , intracellular , plasma membrane ca2+ atpase , biophysics , calcium in biology , membrane potential , chemistry , calcium atpase , t type calcium channel , membrane permeability , cell membrane , trpv6 , voltage dependent calcium channel , biochemistry , biology , cell , membrane , atpase , organic chemistry , enzyme
Removal of extracellular calcium may result in depolarization of the resting cell membrane potential. This has been attributed to the stabilizing action of calcium on the ionic permeability of the cell membrane. It is unknown whether this phenomenon is exclusively mediated by extracellular calcium or through associated changes in intracellular calcium. To examine this, we exposed rat aortic smooth muscle cells in culture to different calcium concentrations and studied their effects on the resting membrane potential and intracellular calcium activity. The resting membrane potential was dependent on the extracellular potassium concentration. Exposure to reduced extracellular calcium concentrations (0.25 and 0.5 mM) caused a steep and reversible depolarization of the membrane potential, but intracellular calcium, measured with fura 2-AM, was not reduced below that measured in control conditions (1.8 mM). Atomic absorption spectrophotometric measurements did not indicate a measurable gain in cell sodium after reduction of extracellular calcium levels. We conclude that extracellular calcium controls the resting cell membrane potential of vascular smooth muscle through a mechanism that is independent of cytosolic Ca2+ activity.

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