Calcium and excitation–contraction coupling in vascular smooth muscles

1982 ◽  
Vol 60 (4) ◽  
pp. 483-488 ◽  
Author(s):  
George B. Weiss

The roles of Ca2+ in excitation–contraction coupling in vascular smooth muscle have been difficult to delineate, primarily because unambiguous association of specific Ca2+ components with morphologically defined cellular structures could not be attained. More recent use of washouts in La3+-substituted solutions at low temperature (to remove superficial Ca2+ and retain cellular Ca2+), Scatchard-coordinate plots (to identify incubation conditions appropriate for examining predominantly high or low affinity Ca2+ components), and high concentrations of Sr2+ (to remove high but not low affinity Ca2+) have facilitated qualitative and quantitative separation of different Ca2+ fractions. The release of high affinity Ca2+ elicited with norepinephrine and the increase in uptake of low affinity Ca2+ obtained with high K+ have been clearly demonstrated, and may directly measure or indirectly reflect changes in the level of intracellular free Ca2+. In other types of vascular smooth muscle (e.g., renal vessels, coronary arteries), similar Ca2+ components also appear to be present, but their relative size and functional importance for regulation of contractile responsiveness can differ.

2005 ◽  
Vol 83 (8-9) ◽  
pp. 725-732 ◽  
Author(s):  
Simon Hirota ◽  
Peter B Helli ◽  
Adriana Catalli ◽  
Allyson Chew ◽  
Luke J Janssen

The primary complaints from patients with asthma pertain to function of airway smooth muscle (ASM) function including shortness of breath, wheezing, and coughing. Thus, it is imperative to better understand the mechanisms underlying excitation-contraction coupling in ASM. Here, we review the various signaling pathways underlying contraction in ASM, and then examine how these are altered in asthma and airway hyperresponsiveness (a hallmark feature of asthma). Throughout, we highlight how studies of vascular smooth muscle have helped or hindered progress in understanding ASM physiology and pathophysiology.Key words: airway smooth muscle, vascular smooth muscle, excitation-contraction coupling, calcium, Rho-kinase.


2009 ◽  
Vol 23 (4-6) ◽  
pp. 407-414 ◽  
Author(s):  
Svetlana V. Koltsova ◽  
Oksana G. Luneva ◽  
Julie L. Lavoie ◽  
Johanne Tremblay ◽  
Georgy V. Maksimov ◽  
...  

2002 ◽  
Vol 119 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Theodor V. Burdyga ◽  
Susan Wray

Moderate cooling of smooth muscle can modulate force production and may contribute to pathophysiological conditions, but the mechanisms underlying its effects are poorly understood. Interestingly, cooling increases force in rat ureter, but decreases it in guinea pigs. Therefore, this study used ureteric smooth muscle as a model system to elucidate the mechanisms of the effects of cooling on excitation-contraction coupling. Simultaneous recordings of force, intracellular [Ca2+], and electrical activity were made in intact ureter and ionic currents measured in isolated cells. The increase in force amplitude in rat ureter with cooling was found to be due to a significant increase in the duration of the Ca2+ transient. This in turn was due to a marked prolongation of the action potential. In guinea pigs, both these parameters were much less affected by cooling. Examination of membrane currents revealed that differences in ion channel contribution to the action potential underlie these differences. In particular, cooling potentiated Ca2+-activated Cl− currents, which are present in rat but not guinea pig ureteric smooth muscle, and prolonged the plateau of the action potential and Ca2+ entry. The force-Ca2+ relationship revealed that the increased duration of the Ca2+ transient was sufficient in the rat, but not in the guinea pig, to overcome kinetic lags produced in both species by cooling and potentiate force. Ca2+ entry and release processes were largely temperature-insensitive, but the rate of relaxation was very temperature-sensitive. Effects of cooling on myosin light chain phosphatase, confirmed in experiments using calyculin A, appear to be the predominant mechanisms affecting relaxation. Thus, smooth muscle is diverse in its response to temperature, even when experimental variables, such as the mode of stimulation, are removed. Although the biochemical and mechanical events accompanying contraction are likely to be affected in similar ways by temperature, differences in electrical events lead to subsequent differences in these processes between smooth muscles.


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