scholarly journals On the Mechanisms Whereby Temperature Affects Excitation-Contraction Coupling in Smooth Muscle

2002 ◽  
Vol 119 (1) ◽  
pp. 93-104 ◽  
Author(s):  
Theodor V. Burdyga ◽  
Susan Wray
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Action Potential ◽  
Guinea Pigs ◽  
Smooth Muscles ◽  
Ionic Currents ◽  
Temperature Sensitive ◽  
Isolated Cells ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

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.

scholarly journals Selective activation of excitation-contraction coupling pathways by ETAand ETBreceptors in guinea-pig tracheal smooth muscle

1999 ◽  
Vol 126 (4) ◽  
pp. 893-902 ◽  
Author(s):  
Takashi Inui ◽  
Haruaki Ninomiya ◽  
Yukio Sasaki ◽  
Maki Makatani ◽  
Yoshihiro Urade ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Tracheal Smooth Muscle ◽  
Selective Activation ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling

Muscarinic excitation-contraction coupling mechanisms in tracheal and bronchial smooth muscles

2001 ◽  
Vol 91 (3) ◽  
pp. 1142-1151 ◽  
Author(s):  
Luke J. Janssen ◽  
Jennifer Wattie ◽  
Hwa Lu-Chao ◽  
Tracy Tazzeo
Keyword(s):  
Smooth Muscle ◽  
Airway Smooth Muscle ◽  
Smooth Muscles ◽  
Rho Kinase ◽  
Cyclopiazonic Acid ◽  
Organ Bath ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Coupling Mechanisms ◽  
Sustained Responses

We investigated the mechanisms underlying muscarinic excitation-contraction coupling in canine airway smooth muscle using organ bath, fura 2 fluorimetric, and patch-clamp techniques. Cyclopiazonic acid (CPA) augmented the responses to submaximal muscarinic stimulation in both tracheal (TSM) and bronchial smooth muscles (BSM), consistent with disruption of the barrier function of the sarcoplasmic reticulum. During maximal stimulation, however, CPA evoked substantial relaxation in TSM but not BSM. CPA reversal of carbachol tone persisted in the presence of tetraethylammoium or high KCl, suggesting that hyperpolarization is not involved; CPA relaxations were absent in tissues preconstricted with KCl alone or by permeabilization with β-escin, ruling out a nonspecific effect on the contractile apparatus. Peak contractions were sensitive to inhibitors of tyrosine kinase (genistein) or Rho kinase (Y-27632). Sustained responses were dependent on Ca2+influx in TSM but not BSM; this influx was sensitive to Ni2+ but not La3+. In conclusion, there are several mechanisms underlying excitation-contraction coupling in airway smooth muscle, the relative importance of which varies depending on tissue and degree of stimulation.

Calcium and excitation–contraction coupling in vascular smooth muscles

1982 ◽  
Vol 60 (4) ◽  
pp. 483-488 ◽  
Author(s):  
George B. Weiss
Keyword(s):  
Smooth Muscle ◽  
Vascular Smooth Muscle ◽  
Relative Size ◽  
Smooth Muscles ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
High K ◽  
Renal Vessels ◽  
Quantitative Separation ◽  
High Concentrations

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.

ERG K+ channels modulate the electrical and contractile activities of gallbladder smooth muscle

2003 ◽  
Vol 284 (3) ◽  
pp. G392-G398 ◽  
Author(s):  
Edward Parr ◽  
Maria J. Pozo ◽  
Burton Horowitz ◽  
Mark T. Nelson ◽  
Gary M. Mawe
Keyword(s):  
Smooth Muscle ◽  
Membrane Potential ◽  
Guinea Pig ◽  
Action Potential ◽  
Resting Membrane Potential ◽  
Plateau Phase ◽  
Related Gene ◽  
K Channels ◽  
Contraction Coupling

The current study was undertaken to test the existence and possible role of ether-a-go-go-related gene 1 (ERG1) protein K+ channels in gallbladder smooth muscle (GBSM). Transcripts encoding ERG1 were detected in human, mouse, and guinea pig GBSM, and ERG1 immunoreactivity was observed in GBSM cells. In intracellular voltage recordings, addition of E-4031 (100 nM–1 μM) or cisapride (100 nM–2 μM) caused concentration-dependent excitation of guinea pig GBSM that was not affected by 500 nM TTX + 5 μM atropine, and E-4031 also depolarized the resting membrane potential. In muscle strip studies, E-4031 either induced phasic contractions or significantly increased the amplitude of phasic contractions in spontaneously active tissues ( P = 0.001). E-4031 also potentiated bethanechol-induced contractions. In conclusion, ERG1 channels are expressed in the GBSM, where they play a role in excitation-contraction coupling probably by contributing to repolarization of the plateau phase of the action potential and to the resting membrane potential.

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