Different electrical responses to vasoactive agonists in morphologically distinct smooth muscle cell types.
- 1 October 1994
- journal article
- research article
- Published by Wolters Kluwer Health in Circulation Research
- Vol. 75 (4) , 733-741
- https://doi.org/10.1161/01.res.75.4.733
Abstract
Vascular smooth muscle cells (SMCs) in the blood vessel wall are frequently heterogeneous in nature, differing in their gross morphology, size, and shape, subcellular organelles, cytoskeleton, and contractile protein composition. In adult rat arterial vessels, two populations of SMCs have been shown to predominate: elongated bipolar cells, representing the majority of cells, and epithelial-like SMCs. We examined the ionic responses of these two types of SMCs, isolated by multiple subculture, to vasoactive stimuli. Elevations in intracellular Na+ and Ca2+ were measured with SBFI and fura 2, respectively, and changes in membrane potential were measured using the potential-sensitive fluorescent probe bis-oxonol. The resting membrane potential of the elongated bipolar cells was less negative than that of the epithelial-like SMCs. Exposure of the elongated SMCs to endothelin 1, alpha-thrombin, or arginine vasopressin induced elevations in [Ca2+]i and [Na+]i and membrane depolarization. Depolarization occurred because of entry of both Na+ and Ca2+, and pharmacological blockade of Cl- or K+ channels did not attenuate the depolarization. In contrast, when [Ca2+]i was elevated by the same agonists in the epithelial-like SMCs there was a pronounced hyperpolarization that appeared to be the consequence of enhanced activity of charybdotoxin-sensitive Ca(2+)-activated K+ channels because it was abolished by charybdotoxin (20 nmol/L), partially attenuated by tetraethylammonium chloride (10 mmol/L), and unaffected by apamin (1 mumol/L), glibenclamide (1 mumol/L), or 4-aminopyridine (5 mmol/L). Chelation of [Ca2+]i also abolished the hyperpolarization; instead, a small depolarization was observed.(ABSTRACT TRUNCATED AT 250 WORDS)Keywords
This publication has 26 references indexed in Scilit:
- Protein Kinase C Inhibits the Ca2+-Activated K+ Channel of Cultured Porcine Coronary Artery Smooth Muscle CellsBiochemical and Biophysical Research Communications, 1993
- Molecular cloning and characterization of 2B7, a rat mRNA which distinguishes smooth muscle cell phenotypes and is identical to osteopontin (secreted phosphoprotein I, 2aR)Biochemical and Biophysical Research Communications, 1991
- Stimulation of non‐selective cation channels providing Ca2+ influx into platelets by platelet‐activating factor and other aggregation inducersEuropean Journal of Biochemistry, 1991
- Computer-driven assessment of ‘immature'-type smooth muscle cells in rabbit aortaJournal Of Hypertension, 1991
- Endothelin-induced increases in vascular smooth muscle Ca2+ do not depend on dihydropyridine-sensitive Ca2+ channels.Journal of Clinical Investigation, 1989
- Growth inhibition by protein kinase C late in mitogenesisNature, 1987
- A novel receptor-operated Ca2+-permeable channel activated by ATP in smooth muscleNature, 1987
- Release and properties of endothelium‐derived relaxing factor (EDRF) from endothelial cells in cultureJournal of Cellular Physiology, 1985
- Developmentally regulated production of platelet-derived growth factor-like moleculesNature, 1984
- Lymphocyte membrane potential assessed with fluorescent probesBiochimica et Biophysica Acta (BBA) - Biomembranes, 1980