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At least 937 records · Page 52Linked to original sources
PubMed1987

The theory of sliding filament models for muscle contraction. I. The two-state model.

The mechanical and thermal properties of Huxley's 1957 sliding filament model for striated muscle contraction are reconsidered, with emphasis on general relationships between two-state models and muscle behaviour. New empirical forms for the rate functions f(x) and g(x) are proposed, which give an improved fit to experiments. A specific procedure, based on the shortening heat, for determining model parameters is described and applied to various choices of rate functions. The change in slope of the tension-velocity curve observed by Katz is shown to require at least one discontinuity in the binding rate f(x), and a general formula is given. The two-state model also gives a symmetric cusp in the ATP-rate vs velocity curve at v = 0. The theory is extended to time-varying situations and applied to transient responses following isometric activation by tetanus (including latency relaxation), and unloaded and after-loaded contractions. The early burst of heat production can also be fitted by assigning appropriate values to the heats of binding and dissociation.

Adenosine Triphosphate↗
PubMed1987

[Calcium regulation of muscle contraction: the molecular regulation mechanisms of contracility].

The role of calcium in muscle activation is described with particular emphasis on interactions occurring between the regulatory proteins troponin-C, troponin-I, actin and myosin. These interactions depend on calcium, but in turn they also influence the calcium binding to troponin-C. They may be affected by short "competitive" peptides whose sequences are similar to the amino-acid sequences on the protein-interaction sites. They may be also affected by certain drugs (cardiotonic calcium sensitizers) that influence the calcium sensitivity of myofilaments.

Animals↗
PubMed1987

Regional and cellular heterogeneity of cholecystokinin receptors mediating muscle contraction in the gut.

The contractile action of cholecystokinin (CCK) on smooth muscle of the gut is either direct (gallbladder and gastric fundus) or both direct and neurally mediated (small intestine). These regional differences were used to characterize pharmacologically CCK receptors on smooth muscle cells and neurons of the gastric fundus, gallbladder, and ileum of the guinea pig. In circular and longitudinal ileal smooth muscle, tetrodotoxin was used to separate direct from neurally mediated contractile effects. Cholecystokinin receptors on smooth muscle cells were found in all locations. The muscle cells displayed a decreasing order of sensitivity to the C-terminal octapeptide of cholecystokinin as expressed in the median doses, and to the selective cholecystokinin antagonist, proglumide, as expressed in the inhibitory dissociation constants. The median doses of the octapeptide of cholecystokinin ranged from 5.5 nM in gallbladder muscle to 185 nM in circular ileal muscle; the corresponding inhibitory dissociation constants of proglumide ranged from 180 to 437 microM [corrected]. Cholecystokinin receptors on cholinergic neurons were confined to circular and longitudinal ileal muscle; the neurons were 80-300 times more sensitive to the octapeptide of cholecystokinin (D50's 0.5 and 2.3 nM) than the corresponding muscle cells, and 19-21 times more sensitive to proglumide (inhibitory dissociation constants, 20 microM [corrected]). The results provide clear evidence of cellular heterogeneity of cholecystokinin receptors (i.e., difference in sensitivity between muscle cells and neurons from the same location) as well as regional heterogeneity (i.e., difference in sensitivity between muscle cells from various locations).

Animals↗
PubMed1993

Calponin: thin filament-linked regulation of smooth muscle contraction.

Calponin is a basic, approximately 34,000 M(r), smooth muscle-specific protein which is developmentally expressed in up to four isoforms. Calponin binds very strongly to actin in a Ca(2+)-independent manner and is localized to the thin filaments in smooth muscle, where it is present at a stoichiometry of 1 mol calponin/7 mol actin. The interaction of calponin with actin inhibits the actomyosin MgATPase (cross-bridge cycling rate) without affecting myosin phosphorylation. The calponin-actin interaction is blocked and calponin-mediated inhibition of the actomyosin MgATPase is reversed upon phosphorylation of calponin by either PKC or CaM kinase II; these properties are restored upon dephosphorylation of calponin by a type 2A protein phosphatase. Consistent with these in vitro findings, calponin is phosphorylated in intact smooth muscle in response to contractile stimuli. The increasing body of evidence, both in vitro and in vivo, strongly supports calponin phosphorylation-dephosphorylation as a thin filament-linked regulatory system in smooth muscle.

Actins↗
PubMed2003

Smooth muscle contraction and relaxation.

This brief review serves as a refresher on smooth muscle physiology for those educators who teach in medical and graduate courses of physiology. Additionally, those professionals who are in need of an update on smooth muscle physiology may find this review to be useful. Smooth muscle lacks the striations characteristic of cardiac and skeletal muscle. Layers of smooth muscle cells line the walls of various organs and tubes in the body, and the contractile function of smooth muscle is not under voluntary control. Contractile activity in smooth muscle is initiated by a Ca(2+)-calmodulin interaction to stimulate phosphorylation of the light chain of myosin. Ca(2+) sensitization of the contractile proteins is signaled by the RhoA/Rho kinase pathway to inhibit the dephosphorylation of the light chain by myosin phosphatase, thereby maintaining force generation. Removal of Ca(2+) from the cytosol and stimulation of myosin phosphatase initiate the process of smooth muscle relaxation.

Calcium↗
PubMed1990

Effect of acetylcholine and morphine on bronchial smooth muscle contraction and its modulation by steroid hormones.

1. The effects of corticosteroid pretreatment on acetylcholine (ACH)-induced contraction of bronchial smooth muscle (BSM) were studied. 2. ACH dose-response curves for dexamethasone (DM)- and corticosterone (B)-treated but not deoxycorticosterone (DOC)-treated BSM were significantly shifted to the right; this provides evidence that glucocorticoid treatment reduced the sensitivity of BSM to ACH. 3. Morphine enhanced BSM contraction in response to ACH by 20%. DM suppressed this enhancement. 4. These findings correlated well with the reduction of muscarinic receptor numbers in BSM by glucocorticoids in our previous study. In addition, glucocorticoids reduced the sensitivity of BSM to opioids.

Acetylcholine↗
PubMed1991

[Synchronization of discharges of human motor units during voluntary muscle contractions and tonic vibration reflex].

Cross-correlograms (CCGs) of action potentials of single motor unit (MU) pairs of soleus, triceps br. and 1 interosseus dors muscles were plotted. The CCGs of 21 pairs from 126 pairs studied during voluntary muscle contraction revealed peaks at a zero point, the peak width being less than or equal to 5 ms (short-term synchronization). During the tonic vibration reflex of the soleus and triceps br. muscles there were 12 synchronized MU pairs from 86 studied pairs. The CCGs of MU 1 and 2 interosseus dors. muscles revealed the synchronization in 4 pairs from 10 studied pairs. The "strength" of synchronization in all MU pairs was low: usually no more than 6% of all impulses coincided above the probability of accidental coincidences. The short-term synchronization is, presumably, a result of common input to different motoneurons from branches of the last-order premotoneuron nerve fibres. The long-term synchronization of MUs was revealed in the CCGs. This synchronization is supposedly caused by the muscle fatigue during the experiment.

Action Potentials↗
PubMed1993

Mediation of anaphylaxis-induced jejunal circular smooth muscle contraction in rats.

Altered intestinal motility and diarrhea are features of food protein-induced intestinal anaphylaxis in the conscious rat. These experiments were performed to determine the mediator(s) responsible for jejunal circular smooth muscle contraction during this response. Hooded-Lister rats were sensitized by intraperitoneal injection of 10-micrograms egg albumin, and controls were sham-sensitized with saline. Fourteen days later the contractility of the circular muscle in jejunal segments (mucosa intact) was examined in standard tissue baths in response to antigen (Ag) or other agents. While control and sensitized tissues contracted in similar fashion in response to stretch, bethanechol, histamine, or 5-hydroxytryptamine (5HT), Ag contracted only the segments of sensitized animals. The contractile response was: (1) specific to the sensitizing Ag, as bovine serum albumin did not induce contraction and (2) could be passively transferred with serum containing specific immunoglobulin E antibody (IgE-Ab). Concanavalin A, which degranulates both mucosal and connective tissue-type mast cells, and compound 48/80, which degranulates only connective tissue-type mast cells produced contractile responses. Ag-induced contraction was significantly inhibited by the mucosal and connective tissue-type mast cell stabilizer doxantrazole, but not the connective tissue mast cell stabilizer disodium cromoglycate. Diphenhydramine and cimetidine together significantly inhibited histamine-induced contraction, but failed to effect the Ag-induced contraction in sensitized tissues. While the contractile response to 5HT was reduced in the presence of methysergide (5HT1-receptor antagonist), cinanserin (5HT2-receptor antagonist), and ICS 205-930 (5HT3-receptor antagonist), only cinanserin significantly inhibited the contractile response to Ag. Indomethacin significantly inhibited Ag-induced contraction. Ag-induced contraction was resistant to atropine and tetrodotoxin.(ABSTRACT TRUNCATED AT 250 WORDS)

Anaphylaxis↗