Alterations of excitation-contraction coupling by platelet-derived growth factor in enzymatically isolated and cultured vascular smooth muscle cells

We studied stimulus-specific alterations of the excitation-contraction coupling pathway in freshly isolated contractile and subcultured non-contractile vascular smooth muscle cells. Using the calcium indicator aequorin, we detected physiological increases in cytoplasmic free calcium [( Ca2+]i) in su...

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Bibliographic Details
Published in:Pflügers Archiv 1985-09, Vol.405 (1), p.77-79
Main Authors: MORGAN, K. G, DEFEO, T. T, WENC, K, WEINSTEIN, R
Format: Article
Language:English
Subjects:
Aequorin
Angiotensin II - pharmacology
Animals
Biological and medical sciences
Cell physiology
Cells, Cultured
Cytological Techniques
Dose-Response Relationship, Drug
Electrophysiology
Fundamental and applied biological sciences. Psychology
Molecular and cellular biology
Muscle, Smooth, Vascular - cytology
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - physiology
Platelet-Derived Growth Factor - pharmacology
Potassium - pharmacology
Rats
Responses to growth factors, tumor promotors, other factors
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Summary:We studied stimulus-specific alterations of the excitation-contraction coupling pathway in freshly isolated contractile and subcultured non-contractile vascular smooth muscle cells. Using the calcium indicator aequorin, we detected physiological increases in cytoplasmic free calcium [( Ca2+]i) in subcultured smooth muscle cells subjected to angiotensin or 33 mM potassium depolarization. These increases were qualitatively identical to those previously measured in intact vascular strips. Platelet-derived growth factor (PDGF) induced a slow, sustained [Ca2+]i increase when applied to the subcultured smooth muscle cells at low picomolar concentrations. Freshly isolated, contractile vascular smooth muscle cells, prepared by a novel technique, exhibited a slow shortening of 20% of resting length in response to PDGF. PDGF also markedly potentiated smooth muscle cell shortening in response to an ED50 dose of phenylephrine. This effect was PDGF concentration dependent. The time course of shortening induced by PDGF alone was consistent with the time course of the PDGF-induced [Ca2+]i increase in the cultured smooth muscle cells. These data suggest that agonists which induce [Ca2+]i changes in contractile smooth muscle cells may retain this ability with respect to cultured smooth muscle cells. PDGF, a peptide mitogen for proliferative smooth muscle cells, may also serve to modulate vascular tone by modestly raising [Ca2+]i in contractile smooth muscle cell and, therefore, sensitizing the cells to alpha adrenergic agonists.
ISSN:0031-6768
1432-2013
DOI:10.1007/BF00591101