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.

Excitation-contraction coupling in multiunit tracheal smooth muscle during metabolic depletion: induction of rhythmicity

1977 ◽  
Vol 233 (1) ◽  
pp. C8-C13 ◽  
Author(s):  
R. Bose ◽  
D. Bose
Keyword(s):  
Smooth Muscle ◽  
Action Potentials ◽  
Tonic Contraction ◽  
Tracheal Smooth Muscle ◽  
Coupling Mechanism ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Osmotic Effect ◽  
Substrate Removal ◽  
Rhythmic Contractions

Multiunit canine tracheal smooth muscle responded to carbachol with graded depolarization and tonic contraction. The same concentration of carbachol, after metabolic depletion by substrate removal, produced rhythmic contractions and action potentials. Similar mechanical effects were also observed with acetylcholine or histamine. These effects were reversed by reintroducing glucose or beta-hydroxybutyrate, but not by 3-O-methylglucose, which is not metabolized; hence, the structural requirements for glucose, per se, or any osmotic effect were ruled out. Sensitivity to extracellular Ca2+ was increased. A Ca2+-influx blocker, D-600, in low concentration (2 X 10(-8) M) abolished the rhythmic contractions without affecting the tonic contraction. Progressive metabolic depletion in presence of carbachol led to fluctuations in membrane potential with a crest of depolarization and appearance of action potentials, each of which resulted in a small contraction. Many of the small contractions partially fused to form the major rhythmic contractions which appeared at a frequency of one per minute. Rhythmicity could not be produced by increasing extracellular K+ concentration (20-120 mM) in presence of atropine (13(-7) M), but instead a tonic contraction occurred. These results suggest changes in excitation-contraction coupling mechanism with agonists like acetylcholine, carbachol, or histamine during substrate deprivation.

scholarly journals Novel role for the transient potential receptor melastatin 4 channel in guinea pig detrusor smooth muscle physiology

2013 ◽  
Vol 304 (5) ◽  
pp. C467-C477 ◽  
Author(s):  
Amy C. Smith ◽  
Kiril L. Hristov ◽  
Qiuping Cheng ◽  
Wenkuan Xin ◽  
Shankar P. Parajuli ◽  
...  
Keyword(s):  
Smooth Muscle ◽  
Guinea Pig ◽  
Transient Receptor Potential ◽  
Critical Role ◽  
Protein Detection ◽  
Muscle Physiology ◽  
Detrusor Smooth Muscle ◽  
Excitation Contraction Coupling ◽  
Contraction Coupling ◽  
Trpm4 Channel

Members of the transient receptor potential (TRP) channel superfamily, including the Ca2+-activated monovalent cation-selective TRP melastatin 4 (TRPM4) channel, have been recently identified in the urinary bladder. However, their expression and function at the level of detrusor smooth muscle (DSM) remain largely unexplored. In this study, for the first time we investigated the role of TRPM4 channels in guinea pig DSM excitation-contraction coupling using a multidisciplinary approach encompassing protein detection, electrophysiology, live-cell Ca2+ imaging, DSM contractility, and 9-phenanthrol, a recently characterized selective inhibitor of the TRPM4 channel. Western blot and immunocytochemistry experiments demonstrated the expression of the TRPM4 channel in whole DSM tissue and freshly isolated DSM cells with specific localization on the plasma membrane. Perforated whole cell patch-clamp recordings and real-time Ca2+ imaging experiments with fura 2-AM, both using freshly isolated DSM cells, revealed that 9-phenanthrol (30 μM) significantly reduced the cation current and decreased intracellular Ca2+ levels. 9-Phenanthrol (0.1–30 μM) significantly inhibited spontaneous, 0.1 μM carbachol-induced, 20 mM KCl-induced, and nerve-evoked contractions in guinea pig DSM-isolated strips with IC50 values of 1–7 μM and 70–80% maximum inhibition. 9-Phenanthrol also reduced nerve-evoked contraction amplitude induced by continuous repetitive electrical field stimulation of 10-Hz frequency and shifted the frequency-response curve (0.5–50 Hz) relative to the control. Collectively, our data demonstrate the novel finding that TRPM4 channels are expressed in guinea pig DSM and reveal their critical role in the regulation of guinea pig DSM excitation-contraction coupling.

Sign in / Sign up

Export Citation Format

Share Document