Endothelin-induced electrical activity and calcium dynamics in vascular smooth muscle cells : A model study

A model is proposed to describe the electrical activity and intracellular calcium dynamics of vascular smooth muscle cells (SMC) induced by endothelin (ET1). The conductance of the nonselective channels (NSCs), proportional to the ET1-receptor complex (ET . R), is intracellular calcium dependent. In...

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Bibliographic Details
Published in:Annals of biomedical engineering 1996-09, Vol.24 (5), p.547-560
Main Authors: WONG, A. Y. K, KLASSEN, G. A
Format: Article
Language:English
Subjects:
Animals
Arteries - physiology
Biological and medical sciences
Calcium - physiology
Computerized, statistical medical data processing and models in biomedicine
Electric Conductivity
Endothelin-1 - pharmacology
Endothelin-1 - physiology
Humans
Medical sciences
Models and simulation
Models, Cardiovascular
Muscle, Smooth, Vascular - drug effects
Muscle, Smooth, Vascular - physiology
Potassium Channels - physiology
Receptors, Endothelin - physiology
Veins - physiology
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Summary:A model is proposed to describe the electrical activity and intracellular calcium dynamics of vascular smooth muscle cells (SMC) induced by endothelin (ET1). The conductance of the nonselective channels (NSCs), proportional to the ET1-receptor complex (ET . R), is intracellular calcium dependent. Inositol (1,4,5)-trisphosphate (IP3) produced by ET1 releases Ca2+ from the IP3-sensitive Ca2+ store. The transient increase of intracellular Ca2+ triggers the release of Ca2+ from the Ca(2+)-sensitive store by a Ca(2+)-induced Ca2+ (CICR) mechanism and activates the Ca(2+)-activated K+ current (IK,Ca). The inward current (Iin) via the NSC can depolarize the cell to a level at which the L-type Ca2+ current becomes activated (ICa). The level of depolarization is determined by the relative amplitude of (Iin + ICa + IK,Ca) and the voltage- and time-dependent K+ current. The model simulations show that (a) in cells without a CICR mechanism, short-lasting stimulation by ET1 elicits higher membrane potential and Ca2+ than long-lasting stimulation; (b) in cells with or without a CICR mechanism, a reduction of normal membrane capacitance (1 muf/cm2) results in either significant and sustaining or oscillatory membrane potential and intracellular calcium concentration. The applicability of the model to the study of electrical activity and calcium dynamics associated with hypercholesterolemia is discussed.
ISSN:0090-6964
1573-9686
DOI:10.1007/bf02684224