Subtypes and excitation-contraction coupling mechanisms for neurokinin receptors in smooth muscle of the guinea-pig Taenia caeci

1991 ◽  
Vol 344 (2) ◽  
pp. 225-234 ◽  
Author(s):  
Judith M. Hall ◽  
Ian K. M. Morton
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Neurokinin Receptors ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Coupling Mechanisms

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

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.

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.

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