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PubMed1985

Molecular heterogeneity of leukotriene receptors: correlation of smooth muscle contraction and radioligand binding in guinea-pig lung.

The [3H]leukotriene C4 ([3H]LTC4) and [3H]leukotriene D4 ([3H] LTD4) specific binding sites in guinea-pig lung membranes were characterized and correlated with smooth muscle contractile activities of a series of LTC-, D- and E-type analogs. [3H]LTC4 bound to the specific sites with high affinity (dissociation constant Kd = 15 +/- 5 nM), saturable capacity (maximum binding = 68 +/- 15 pmol/mg of membrane protein), stereoselectivity and specificity. The [3H]LTC4 specific binding sites were detected in the membranes isolated from leukotriene sensitive (e.g., lung and heart) or insensitive (e.g., brain and red blood cells) tissues. [3H] LTD4 also bound to specific sites with high affinity (Kd = 0.20 +/- 0.05 nM), low capacity (maximum binding = 1.1 +/- 0.2 pmol/mg of membrane protein) stereoselectivity and specificity. The [3H] LTD4 specific binding sites were detected in the membranes isolated from lung and trachea. [3H]LTC4 specific binding was inhibited by treatment of the membranes with the sulfhydryl alkylating agent N-ethylmaleimide. [3H]LTD4 specific binding was more sensitive to heat treatment and p-hydroxymercuribenzoate than the [3H]LTC4 specific binding. Radioligand competition activities of the LTD- and LTE-type analogs correlated well with the agonist and antagonist smooth muscle contractile activities. In contrast, the radioligand competition activity of the LTC-type analogs did not correlate with smooth muscle contractile activities. These results indicate that the [3H]LTC4 and [3H]LTD4 specific binding sites in guinea-pig lung membranes are chemically and physically distinct. The [3H]LTD4 specific binding sites represent physiologically and pharmacologically important receptors, and the smooth muscle contraction induced by LTD-, and possible LTE-, type analogs are mediated through the LTD4 receptors.

Animals↗
PubMed1985

Smooth muscle contraction bands in the media of coronary arteries: a postmortem marker of antemortem coronary spasm?

To date, no unequivocal morphologic markers have been described that would allow the diagnosis of coronary artery spasm to be made at autopsy. The coronary arteries of 63 adult patients without myocardial infarction were examined at autopsy, and the presence of medial smooth muscle contraction bands in these vessels was correlated with other vascular changes, myocardial pathologic changes and clinical history. These contraction bands have not been reported previously in human coronary arteries, but they were identified in experimental vascular spasm induced with catecholamines. It was found that 47 of the 63 cases were positive for contraction bands. As evidence of an antemortem process, there was a significant correlation between these changes and the presence of nonocclusive microthrombi, found in 25 cases. Contraction bands were also highly correlated with atherosclerotic plaque ruptures and mural plaque hemorrhages, which may be secondary to coronary spasm. In 78.7% of the cases positive for contraction bands, the cause of death was related to a diagnosis possibly associated with high catecholamine levels. On the basis of experimental evidence and the correlations identified in this study, coronary artery medial smooth muscle contraction bands may represent a postmortem marker of antemortem coronary spasm.

Adult↗
PubMed1999

Molecular model of muscle contraction.

A quantitative stochastic model of the mechanochemical cycle of myosin, the protein that drives muscle contraction, is proposed. It is based on three premises: (i) the myosin head incorporates a lever arm, whose equilibrium position adjusts as each of the products of ATP hydrolysis dissociates from the nucleotide pocket; (ii) the chemical reaction rates are modified according to the work done in moving the arm; and (iii) the compliance of myosin's elastic element is designed to permit many molecules to work together efficiently. The model has a minimal number of parameters and provides an explanation, at the molecular level, of many of the mechanical and thermodynamic properties of steadily shortening muscle. In particular, the inflexion in the force-velocity curve at a force approaching the isometric load is reproduced. Moreover, the model indicates that when large numbers of myosin molecules act collectively, their chemical cycles can be synchronized, and that this leads to stepwise motion of the thin filament. The oscillatory transient response of muscle to abrupt changes of load is interpreted in this light.

Animals↗
PubMed2003

Ca2+ antagonist-insensitive coronary smooth muscle contraction involves activation of epsilon-protein kinase C-dependent pathway.

Certain angina and coronary artery disease forms do not respond to Ca2+ channel blockers, and a role for vasoactive eicosanoids such as PGF2alpha in Ca2+ antagonist-insensitive coronary vasospasm is suggested; however, the signaling mechanisms are unclear. We investigated whether PGF2alpha-induced coronary smooth muscle contraction is Ca2+ antagonist insensitive and involves activation of a PKC-dependent pathway. We measured contraction in single porcine coronary artery smooth muscle cells and intracellular free Ca2+ concentration ([Ca2+]i) in fura 2-loaded cells and examined cytosolic and particulate fractions for PKC activity and reactivity with isoform-specific PKC antibodies. In Hanks' solution (1 mM Ca2+), PGF2alpha (10-5 M) caused transient [Ca2+]i increase followed by maintained [Ca2+]i increase and 34% cell contraction. Ca2+ channel blockers verapamil and diltiazem (10-6 M) abolished maintained PGF2alpha-induced [Ca2+]i increase but only partially inhibited PGF2alpha-induced cell contraction to 17%. Verapamil-insensitive PGF2alpha contraction was inhibited by PKC inhibitors GF-109203X, calphostin C, and epsilon-PKC V1-2. PGF2alpha caused Ca2+-dependent alpha-PKC and Ca2+-independent epsilon-PKC translocation from cytosolic to particulate fractions that was inhibited by calphostin C. Verapamil abolished PGF2alpha-induced alpha-but not epsilon-PKC translocation. PMA (10-6 M), a direct activator of PKC, caused 21% contraction with no significant [Ca2+]i increase and epsilon-PKC translocation that were inhibited by calphostin C but not verapamil. Membrane depolarization by 51 mM KCl, which stimulates Ca2+ influx, caused 36% cell contraction and [Ca2+]i increase that were inhibited by verapamil but not GF-109203X or calphostin C and did not cause alpha- or epsilon-PKC translocation. Thus a significant component of PGF2alpha-induced contraction of coronary smooth muscle is Ca2+ antagonist insensitive, involves Ca2+-independent epsilon-PKC activation and translocation, and may represent a signaling mechanism of Ca2+ antagonist-resistant coronary vasospasm.

Animals↗
PubMed2006

Teaching from classic papers: Hill's model of muscle contraction.

A. V. Hill's 1938 paper "The heat of shortening and the dynamic constants of muscle" is an enduring classic, presenting detailed methods, meticulous experiments, and the model of muscle contraction that now bears Hill's name. Pairing a simulation based on Hill's model with a reading of his paper allows students to follow his thought process to discover key principles of muscle physiology and gain insight into how to develop quantitative models of physiological processes. In this article, the experience of the author using this approach in a graduate biomedical engineering course is outlined, along with suggestions for adapting this approach to other audiences.

History, 20th Century↗
PubMed1994

Laryngeal movement, oropharyngeal pressure, and submental muscle contraction during swallowing.

This study examined temporal relationships of laryngeal movement, oropharyngeal pressure and submental muscle contraction during swallowing. Techniques used to obtain the temporal measures were electroglottography (EGG), oropharyngeal manometry, and submental surface electromyography. Liquid bolus swallows were performed by 40 normal subjects evenly divided by young and elderly, men and women. Results of this investigation suggest that the EGG waveform is reflective of the temporal aspects of laryngeal movement during swallowing and that the EGG has potential as a behavioral modification technique in swallowing therapy. A case study is presented to illustrate the use of the electroglottograph for biofeedback.

Adult↗
PubMed1987

Pupillary sympathetic hypofunction and asymmetry in muscle contraction headache and migraine.

Pupillary autonomic dysfunction and right-left differences were investigated in muscle contraction headache (MCH) and migraine, by means of biocular infrared videopupillography (biocular Iriscorder). The study was performed on 36 patients with MCH or migraine and on 23 healthy controls. The pupillary area before light stimuli and maximum dilatation velocity of pupils, in MCH patients and migraineurs, showed significant differences from those of controls. Pupillary asymmetry was observed in both headache categories. The behavior of MCH pupils to light stimuli under dark conditions was rather similar to that of migraine pupils. Both pupillary sympathetic hypofunction and subtle anisocoria were present not only in patients with migraine but also in those with MCH.

Adolescent↗
PubMed1998

Involvement of small GTPases in the regulation of smooth muscle contraction.

Neurohumoral stimulation of smooth muscle leads to an increased responsiveness of the myofilaments to Ca2+. This review provides a summary of the data that suggest that the signalling from the membrane-bound serpentine receptors to the contractile apparatus leading to the increase in Ca(2+)-sensitivity requires the activation of the Ras-related low molecular mass GTPase Rho. In smooth muscle permeabilized with alpha-toxin or beta-escin, the increase in force elicited by different agonists at fixed [Ca2+] (Ca(2+)-sensitization) can be inhibited by bacterial toxins (EDIN, and exoenzyme C3) which ADP-ribosylate and inactivate Rho proteins. Moreover, the agonist-induced increase in Ca(2+)-sensitivity can be mimicked by constitutively active recombinant Rho proteins. The physiological relevance of this mechanism is suggested by the fact that toxins that are internalized into intact cells (toxin B from C. difficile and a chimeric toxin (DC3B) consisting of C3 and the (non-catalytic) B fragment of diphteria toxin (inhibit the tonic phase of an agonist-induced contraction. Toxin B inhibits contraction without affecting the intracellular Ca(2+)-transient determined with fura-2. However, it inhibits phosphorylation of the regulatory light chains of myosin (MLC). Rho has been suggested to activate a Rho-associated kinase which in turn phosphorylates the myosin binding subunit of the myosin light chain phosphatase. This would lead to an increase in phosphorylation of MLC and hence of force at constant Ca2+. The Ca(2+)-sensitizing effect of agonists is also inhibited by tyrosine kinase inhibitors. This suggests the possibility that in smooth muscle, like in non-muscle cells, there is a cross-talk between Rho and tyrosine kinases.

Actin Cytoskeleton↗
PubMed1993

Regulation of vascular smooth muscle contraction by extracellular Na+.

1. The effects of extracellular Na+ removal on agonist-induced contraction of vascular smooth muscle in vitro are reviewed. 2. The effects of extracellular Na+ removal on contraction vary depending upon the agonist and vessel. 3. Factors that may influence the effects of extracellular Na+ removal on agonist-induced contraction include the compound substituted for Na+, time of tissue exposure to lowered extracellular Na+, concentration of extracellular Na+, agonist concentration, presence of the vascular endothelium and presence of basal tone. 4. The potential influence of these factors needs to be determined and minimized, in studies that investigate the role of extracellular Na+ in agonist-induced contraction.

Animals↗
PubMed1994

The role of active smooth-muscle contraction in the occurrence of chronic vasospasm in the canine two-hemorrhage model.

To evaluate the pathogenetic role of alterations in the physical properties of the arterial wall (the passive component) and of active smooth-muscle contraction (the active component) in the occurrence of chronic vasospasm, the temporal profiles of these events were examined using the canine "two-hemorrhage" model. In the in vivo study, the basilar artery was exposed via the transclival approach on Day 0, 2, 4, 7, or 14. Nicardipine, followed by the protein kinase C inhibitor H-7, then papaverine were administered in a cumulative fashion, and the change in the basilar artery diameter induced by the addition of each agent was recorded angiographically. Drug administration markedly reversed the arterial narrowing caused by chronic vasospasm. When the vasodilatory effect of each agent was compared, the dilation induced by nicardipine or papaverine progressively decreased from Day 2 to Day 7, whereas that induced by H-7 increased. The in vitro experiment using arterial segments excised from the basilar artery revealed a progressive increase in arterial stiffness from Day 2 to Day 7. Also, there was a significant decrease in the initial half-circumference of the arterial segment, which was at its maximum on Days 4 and 7. However, the alteration in the initial half-circumference was considerably less than that in the angiographic diameter following subarachnoid hemorrhage. These data indicate that the augmented spontaneous tonus of the smooth muscle plays the predominant role in the occurrence of chronic vasospasm. Thus, the involvement of the protein kinase C-mediated contractile system is strongly suggested.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed1991

Responses of upper airway muscles to gastrocnemius muscle contraction in dogs.

We studied electromyographic (EMG) responses of the alae nasi (AN) and the posterior cricoarytenoid (PCA) muscles, which act as upper airway dilators, during contraction of gastrocnemius muscle in six chest-intact anesthetized dogs with spontaneous breathing and in four thoracotomized, phrenicotomized and mechanically ventilated dogs with right thoracic and left cervical vagotomy. Muscle contraction was phasically induced by electrical stimulation of the intact gastrocnemius nerve or the distal cut end of this nerve for 20-30 sec. Stimulation intensity was determined as twice the motor threshold in each dog. In chest-intact animals, phasic contraction induced by intact nerve stimulation produced initial rapid increases in upper airway muscle activity, but stimulation of the distal cut end of the nerve did not show the rapid increase in upper airway muscle activity. Furthermore, stimulation of the proximal cut end did not produce any transient response with the stimulation intensity used in this study. In chest-open and vagotomized animals with artificial ventilation, responses of the upper airway muscles to contraction during the intact nerve stimulation were observed. These results suggest that the contraction of the gastrocnemius muscle activates upper airway dilating muscles via reflex mechanisms.

Afferent Pathways↗
PubMed1987

Comparison of the effectiveness of two pelvic stabilization systems on pelvic movement during maximal isometric trunk extension and flexion muscle contractions.

The purpose of this study was to compare the effectiveness of two pelvic fixation systems to limit pelvic movement during isometric trunk extension and flexion muscle strength testing. We developed a prototypal pelvic fixation system and compared it with a pelvic strap stabilization system. The prototypal pelvic fixation system consisted of fixation of the anterior superior iliac spines and sacrum, and the pelvic strap stabilization system consisted of a strap across the anterior superior iliac spines and a posterior pad. Small, but statistically significant, pelvic position changes occurred during isometric trunk extension and flexion muscle strength testing with the two stabilization systems. The pelvic angle changes were greater in extension than in flexion and greater when only the pelvic strap stabilization system rather than the prototypal pelvic fixation system was used. Our findings indicate that a more extensive prototypal pelvic fixation system minimizes pelvic movement to a greater extent during isometric trunk extension and flexion muscle contractions compared with the strap stabilization system.

Abdominal Muscles↗
PubMedDate not supplied

Augmented sensory nerve action potentials during distant muscle contraction.

We previously reported that the median sensory nerve action potentials (SNAP) increased in amplitude during ipsilateral abductor pollicis brevis contraction. The objectives of the present project were to study the timing and origin of this phenomenon and to eliminate the possibility of local artifact. Ten normal subjects were recruited. The baseline was established using ten threshold stimuli, which were delivered to the median nerve at the wrist at 0.2 Hz. Using the same stimulus strength, the SNAP was recorded while the tibialis anterior was contracted at 25, 50, 75, and 100% of maximum force. Responses were signal-averaged. Results showed an increase in ipsilateral SNAP amplitude between baseline and maximum contraction of 6 +/- 2 microV (standard error, P = 0.004) and contralateral amplitude of 8 +/- 2 microV (standard error, P = 0.01). Statistical analysis was performed with analysis of variance for repeated measures and paired t test. The effect peaked between 0 and 10 min after contraction and lasted from 1.5 to more than 20 min after muscle relaxation. In conclusion, SNAP appear to be enhanced during and after muscle contraction. Theories concerning underlying causes for this event are discussed.

Adult↗
PubMed1996

Influence of hyoepiglotticus muscle contraction on canine upper airway geometry.

We examined the effect of hyoepiglotticus (HE) muscle contraction on epiglottic position in 4 anaesthetised (IV choralose, pentobarbitone sodium) tracheostomised, mechanically ventilated dogs studied in the prone mouth open position. Computerised axial tomography (coronal plane) was used to measure the vertical distance between the tip of the epiglottis (E) and (1) the soft palate (SP) (i.e. E-SP distance) and (2) the dorsal wall of the nasopharynx (N) (i.e. E-N distance). Duplicate runs of graded electrical stimulation of the HE muscle, using bilateral bipolar fine wire electrodes, were performed in each animal and resulted in a progressive increase in both the E-SP distance (baseline of 0.5 +/- 0.5 to a maximum of 13.1 +/- 2.3 mm, mean +/- SE) and the E-N distance (29.1 +/- 2.0 to a maximum of 42.2 +/- 2.7 mm, both p < 0.02). We conclude that HE contraction moves the epiglottis ventrally away from the soft palate thus opening and enlarging the oral pathway for airflow.

Animals↗
PubMed2004

Familial hypertrophic cardiomyopathy mutations from different functional regions of troponin T result in different effects on the pH and Ca2+ sensitivity of cardiac muscle contraction.

To understand the molecular function of troponin T (TnT) in the Ca(2+) regulation of muscle contraction as well as the molecular pathogenesis of familial hypertrophic cardiomyopathy (FHC), eight FHC-linked TnT mutations, which are located in different functional regions of human cardiac TnT (HCTnT), were produced, and their structural and functional properties were examined. Circular dichroism spectroscopy demonstrated different secondary structures of these TnT mutants. Each of the recombinant HCTnTs was incorporated into porcine skinned fibers along with human cardiac troponin I (HCTnI) and troponin C (HCTnC), and the Ca(2+) dependent isometric force development of these troponin-replaced fibers was determined at pH 7.0 and 6.5. All eight mutants altered the contractile properties of skinned cardiac fibers. E244D potentiated the maximum force development without changing Ca(2+) sensitivity. In contrast, the other seven mutants increased the Ca(2+) sensitivity of force development but not the maximal force. R92L, R92W, and R94L also decreased the change in Ca(2+) sensitivity of force development observed on lowering the pH from 7 to 6.5, when compared with wild type TnT. The examination of additional mutants, H91Q and a double mutant H91Q/R92W, suggests that mutations in a region including residues 91-94 in HCTnT can perturb the proper response of cardiac contraction to changes in pH. These results suggest that different regions of TnT may contribute to the pathogenesis of TnT-linked FHC through different mechanisms.

Calcium↗
PubMed1993

Suppression of intestinal smooth muscle contraction by 4-ethylguaiacol, a constituent of wood creosote.

Wood creosote, a mixture of phenolic compounds, suppresses in vitro contractions of rat intestine. To identify a compound in wood creosote able to inhibit intestinal motility, we screened its constituent phenolic compounds and found 4-ethylguaiacol (4-EG) as an active compound. It suppressed the spontaneous phasic (IC50 = 513 +/- 48 mumol/l) as well as spasmogenic-agent-induced tonic longitudinal contractions of isolated rat ileum in a reversible and concentration-dependent manner. KCl-depolarization-induced tonic contraction, which was susceptible to a calcium channel blocking agent, was also suppressed by 4-EG with an IC50 of 433 +/- 41 mumol/l. Furthermore, calcium-ionophore-induced contraction, which was affected by an influx of extracellular calcium ion that bypassed calcium channels, was suppressed by 4-EG with an IC50 of 97 +/- 18 mumol/l. These results support the concept that the effect of wood creosote to suppress intestinal motility is attributable, partially or entirely, to its component 4-EG and that this effect of 4-EG on the intestinal muscle is produced at some stage(s) of the muscle contraction process after influx of extracellular calcium into the cytosol of smooth muscle.

Animals↗