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PubMed1998

A strain-dependent ratchet model for [phosphate]- and [ATP]-dependent muscle contraction.

A minimal strain-dependent ratchet model of muscle cross-bridge action is proposed which is broadly compatible with structural and kinetic constraints. Its essential features are: (1) dynamic binding of the S1-products complex to actin through a disorder-order transition coupled to the release of inorganic phosphate; (2) the absence of a force-generating rotation of the myosin head between the two force-holding states A.M.ADP and A.M; (3) strain-control of ADP release and ATP binding, giving net isometric tension and directed motility by the selective dissociation of negatively strained bound states. With a disordered pre-force state, the binding rate to state A.M.ADP need not be symmetric in x, the actin site displacement. With faster binding at positive x, the model predicts many steady-state and transient properties of striated muscle observed experimentally, including phases 2-4 of tension recovery from length changes and their dependence on excess phosphate (which enhances and accelerates phase 3) and reduced ATP (which gives a bimodal phase 2 and slows one mode). The response to large perturbations is often sensitive to the number of actin sites used, and to the inclusion of a 1 nm displacement of the neck region on release of ADP. The latter stabilizes the periodic tension behaviour produced by repeated releases.

Adenosine Triphosphate↗
PubMed1992

Neutral endopeptidase inhibitor potentiates endothelin-1-induced airway smooth muscle contraction.

To study the role of neutral endopeptidase (NEP) on endothelin-1-induced contraction of the airway smooth muscle, we examined the contractile effect of endothelin-1 in the isolated guinea pig trachea and human bronchus in the presence or absence of NEP inhibitor phosphoramidon. After incubation with phosphoramidon (10(-8) to 10(-5) M), we added endothelin-1 cumulatively from 10(-11) to 10(-7) M to the airway tissues in organ baths. Phosphoramidon significantly potentiated the endothelin-1-induced contraction in a concentration-dependent fashion in both guinea pig trachea and human bronchus, and it shifted the concentration-response curves to the left. Because NEP is known to cleave tachykinins, we next studied whether endothelin-1 contracts airway tissues by releasing endogenous tachykinins from bronchial C-fibers. After incubation with phosphoramidon (10(-5) M), we added endothelin-1 cumulatively from 10(-11) to 10(-7) M to the tissues that were treated with capsaicin to deplete the tachykinins. Phosphoramidon significantly potentiated the endothelin-1-induced contraction in the capsaicin-treated tissues, suggesting that endothelin-1 causes the contraction, at least in part, without releasing tachykinins. In contrast to the effect of phosphoramidon, captopril (an angiotensin-converting enzyme inhibitor), leupeptin (a serine protease inhibitor), and bestatin (an aminopeptidase inhibitor) did not modulate the effect of endothelin-1-induced contraction in both guinea pig trachea and human bronchus. From these results, we conclude that NEP plays an important role in regulating endothelin-1-induced contraction in the guinea pig trachea and human bronchus.

Animals↗
PubMed2004

Pacemaker activity from submucosal interstitial cells of Cajal drives high-frequency and low-amplitude circular muscle contractions in the mouse proximal colon.

The present study was aimed at elucidating how pacemaker activity (plateau potentials) (mean frequency: 15.9 +/- 2.8 times min(-1)) from submucosal interstitial cells of Cajal (ICC-SM) control spontaneous contractions in the mouse proximal colon. Mechanical activities in the circular muscle direction showed high-frequency (mean frequency: 15.6 +/- 2.7 times min(-1)) and low-amplitude (mean amplitude: 0.01 +/- 0.005 g) (HFLA) rhythmic contractions. Simultaneous recordings of circular muscle mechanical activity and electrical activity from ICC-SM revealed that HFLA contractions were synchronized with plateau potentials (mean frequency: 15.9 +/- 2.8 times min(-1)). Although low-frequency (3.5 +/- 2.1 times min(-1)) and high-amplitude (0.12 +/- 0.03 g) (LFHA) contractions in both longitudinal and circular muscle directions were synchronized with burst of action potentials in both muscle cells, these LFHA contractions were not synchronous with plateau potentials. Intracellular Ca2+ release from the internal stores through IP3 receptors is not a major factor to generate both action potentials differently from plateau potentials. Neither tetrodotoxin nor atropine affected the plateau potentials. The results reveal that the pacemaker activity from ICC-SM drives only the spontaneous HFLA (one-tenth amplitude of the LFHA circular and longitudinal muscle contractions) circular muscle contractions without control by enteric nerves.

Animals↗
PubMed1984

Thin filament proteins and thin filament-linked regulation of vertebrate muscle contraction.

Recent developments in the field of myofibrillar proteins will be reviewed. Consideration will be given to the proteins that participate in the contractile process itself as well as to those involved in Ca-dependent regulation of striated (skeletal and cardiac) and smooth muscle. The relation of protein structure to function will be emphasized and the relation of various physiologically and histochemically defined fiber types to the proteins found in them will be discussed.

Actins↗