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At least 721 records · Page 40Linked to original sources
PubMed1986

Mechanism of smooth muscle contraction: relevance to safety of beta-adrenergic blockade in hypertensive patients with reversible chronic obstructive airways disease.

The phosphorylation hypothesis of smooth muscle contraction relates formation of cyclic AMP, resulting from beta-adrenergic stimulation, to inhibition of myosin light-chain phosphorylation and hence to bronchial relaxation. The hypothesis can therefore explain why beta-adrenergic blockade promotes bronchospasm in susceptible individuals. In the light of this molecular schema, various novel approaches to the use of beta-adrenergic blocking therapy for hypertension in the presence of asthma are discussed.

Adrenergic beta-Antagonists↗
PubMed1992

Endothelin ETA and ETB receptors mediate vascular smooth muscle contraction.

1. We have investigated the receptors mediating endothelin-induced contraction of rabbit isolated jugular vein (RJV) and rat isolated thoracic aorta (RTA). 2. Endothelin-1 (ET-1) and endothelin-3 (ET-3) contracted RJV preparations with similar potency (EC50 values approximately 1 nM), whereas, ET-1 (EC50:4.5 nM) was approximately 80 fold more potent than ET-3 in contracting RTA. In addition, the ETB receptor-selective agonist [Ala1,3,11,15]ET-1 contracted RJV (EC50:2.1 nM) but not RTA. 3. The ETA receptor antagonist, BQ123, competitively antagonized (pA2 6.93) the contraction of RTA produced by ET-1, but had no effect (at 10 microM) on the contractile effects of either ET-1, ET-3 or [Ala1,3,11,15]ET-1 in RJV. 4. These data suggest that both ETA and ETB receptors can mediate vascular smooth muscle contraction.

Animals↗
PubMed2006

Role of calcium influx through voltage-operated calcium channels and of calcium mobilization in the physiology of Schistosoma mansoni muscle contractions.

We tested the hypothesis that voltage-operated Ca2+ channels mediate an extracellular Ca2+ influx in muscle fibres from the human parasite Schistosoma mansoni and, along with Ca2+ mobilization from the sarcoplasmic reticulum, contribute to muscle contraction. Indeed, whole-cell voltage clamp revealed voltage-gated inward currents carried by divalent ions with a peak current elicited by steps to +20 mV (from a holding potential of -70 mV). Depolarization of the fibres by elevated extracellular K+ elicited contractions that were completely dependent on extracellular Ca2+ and inhibited by nicardipine (half inhibition at 4.1 microM). However these contractions were not very sensitive to other classical blockers of voltage-gated Ca2+ channels, indicating that the schistosome muscle channels have an atypical pharmacology when compared to their mammalian counterparts. Futhermore, the contraction induced by 5 mM caffeine was inhibited after depletion of the sarcoplasmic reticulum either with thapsigargin (10 microM) or ryanodine (10 microM). These data suggest that voltage-operated Ca2+ channels do contribute to S. mansoni contraction as does the mobilization of stored Ca2+, despite the small volume of sarcoplasmic reticulum in schistosome smooth muscles.

Animals↗
PubMed2003

Inhibition of sustained smooth muscle contraction by PKA and PKG preferentially mediated by phosphorylation of RhoA.

The role of RhoA in myosin light-chain (MLC)(20) dephosphorylation and smooth muscle relaxation by PKA and PKG was examined in freshly dispersed and cultured smooth muscle cells expressing wild-type RhoA, constitutively active Rho(V14), and phosphorylation site-deficient Rho(A188). Activators of PKA (5,6-dichloro-1-beta-ribofuranosyl benzimidazole 3',5'-cyclic monophosphothionate, Sp-isomer; cBIMPS) or PKG [8-(4-chlorophenylthio)guanosine 3',5'-cyclic monophosphate (8-pCPT-cGMP), sodium nitroprusside (SNP)] or both PKA and PKG (VIP) induced phosphorylation of constitutively active Rho(V14) and agonist (ACh)- or GTPgammaS-stimulated wild-type RhoA but not Rho(A188). Phosphorylation was accompanied by translocation of membrane-bound wild-type RhoA and Rho(V14) to the cytosol and complete inhibition of ACh-stimulated Rho kinase and phospholipase D activities, RhoA/Rho kinase association, MLC(20) phosphorylation, and sustained muscle contraction. Each of these events was blocked depending on the agent used, by the PKG inhibitor KT5823 or the PKA inhibitor myristoylated PKI. Inhibitors were used at a concentration (1 microM) previously shown by direct measurement of kinase activity to selectively inhibit the corresponding kinase. In muscle cells overexpressing the active phosphorylation site-deficient mutant Rho(A188), MLC(20) phosphorylation was partly inhibited by SNP, VIP, cBIMPS, and 8-pCPT-cGMP, suggesting the existence of an independent inhibitory mechanism downstream of RhoA. Results demonstrate that dephosphorylation of MLC(20) and smooth muscle relaxation are preferentially mediated by PKG- and PKA-dependent phosphorylation and inactivation of RhoA.

Acetylcholine↗
PubMed1992

Effect of chronic renal failure on skeletal and diaphragmatic muscle contraction.

The changes in muscle mechanical properties caused by the myopathy of chronic uremia was examined in the soleus and the diaphragm muscles of rats in which chronic uremia was produced by subtotal nephrectomy. Using an in vitro muscle preparation in two groups of rats (moderately and severely uremic), we determined that uremia had a significant detrimental effect on both muscles with respect to the force-frequency relationships. In the diaphragm it decreased by 15% in the moderate group and by 43% in the severe group. In the soleus it decreased by 20% in both groups. Twitch characteristics behaved differently in the soleus and the diaphragm muscles in that 1/2 RT and TPT increased significantly (p < 0.05) in the soleus (severely uremic group) but not in the diaphragm. Fatigability was increased in both muscles in the moderately uremic rats and in the diaphragm in the severely uremic rats; however, the fatigability of the soleus in the severely uremic group was not different from that in the control group. Our findings suggest that the myopathic changes occurring in chronic uremia affects the function of the soleus and the diaphragm in different ways. Other findings in the severely uremic group indicate that additional factors such as marked electrolyte imbalances may also affect the excitation-contraction coupling in different ways.

Animals↗
PubMed2005

The latch-bridge hypothesis of smooth muscle contraction.

In contrast to striated muscle, both normalized force and shortening velocities are regulated functions of cross-bridge phosphorylation in smooth muscle. Physiologically this is manifested as relatively fast rates of contraction associated with transiently high levels of cross-bridge phosphorylation. In sustained contractions, Ca2+, cross-bridge phosphorylation, and ATP consumption rates fall, a phenomenon termed "latch". This review focuses on the Hai and Murphy (1988a) model that predicted the highly non-linear dependence of force on phosphorylation and a directly proportional dependence of shortening velocity on phosphorylation. This model hypothesized that (i) cross-bridge phosphorylation was obligatory for cross-bridge attachment, but also that (ii) dephosphorylation of an attached cross-bridge reduced its detachment rate. The resulting variety of cross-bridge cycles as predicted by the model could explain the observed dependencies of force and velocity on cross-bridge phosphorylation. New evidence supports modifications for more general applicability. First, myosin light chain phosphatase activity is regulated. Activation of myosin phosphatase is best demonstrated with inhibitory regulatory mechanisms acting via nitric oxide. The second modification of the model incorporates cooperativity in cross-bridge attachment to predict improved data on the dependence of force on phosphorylation. The molecular basis for cooperativity is unknown, but may involve thin filament proteins absent in striated muscle.

Animals↗
PubMed1983

Leukotriene C4 and dimethylphenylpiperazinium-induced responses in canine airway tracheal muscle contraction and fluid secretion.

Leukotrienes have been implicated as putative mediators in several air way diseases. In previous canine studies it was shown that leukotriene C4 (LTC4) enhanced fluid secretion over baseline values and this enhancement could be blocked by hexamethonium. This indicates that leukotrienes have as one of their actions, stimulation of ganglionic motor neurons. In the present study, we determined that LTC4 acts at a similar site as the specific nicotinic receptor agonist dimethylphenylpiperazinium (DMPP). Both LTC4 and DMPP when given alone enhanced mucus secretion and induced tracheal muscle contraction over control baseline (p less than 0.05). When added to DMPP, LTC4 enhanced the DMPP effect of muscle contraction at 5 and 8 micrograms by a synergistic amount, while the secretion was only additive. The slopes of the dose-response curves for DMPP + LTC4 did not differ by a statistically significant amount. LTC4 and DMPP act on a similar, if not the same, ganglionic receptor.

Animals↗
PubMed1988

Catecholamine-associated smooth muscle contraction bands in the media of coronary arteries of brain-dead baboons.

In the brain death baboon model, the baboon experiences an autonomic storm with release of catecholamines both from the adrenal glands and from intracardiac sympathetic nerve endings. Since catecholamines may induce coronary arterial spasm, we looked for morphologic evidence of smooth muscle damage in the coronary arteries of 11 baboons that underwent induction of brain death under general anesthesia. Nine (82%) of the 11 animals showed coronary arterial smooth muscle contraction bands, and 9 (82%) of the 11 baboons also showed focal myocardial contraction bands and myocytolytic necrosis. Focal coronary arterial smooth muscle cell necrosis with intracytoplasmic calcium deposits were observed in three (33%) of the nine contraction band-positive cases. This study provides further support for the concept that medial smooth muscle contraction bands may be a morphologic marker of antemortem coronary arterial spasm.

Animals↗
PubMed2001

Cooling-induced gastrointestinal smooth muscle contractions in the rat.

The aim of this study was to assess the effect of cooling on smooth muscle contraction in various parts of the gastrointestinal tract (esophagus, stomach, duodenum, jejunum and colon) and to investigate the basic mechanism underlying cooling-induced (CIC) tonic and rhythmic contractions. Recordings of isometric tension from smooth muscle strips of different parts of the rat gastrointestinal tract were performed using organ-bath techniques, and stepwise cooling was applied. Cooling was tested before and after the addition of various standard agents interfering with known neurogenic (autonomic blockers, tetrodotoxin, capsaicin) and myogenic mechanisms of contraction (calcium channel blockers, Sarcoplasmatic and Ca2+-ATPase pump inhibitors). Step-wise cooling (37 degrees C to 5 degrees C) of all gastrointestinal smooth muscle preparations induced reproducible graded tonic contractions, inversely proportional to temperature. CIC was most pronounced in the jejunum. Cooling abolished rhythmic smooth muscle activity. CIC was not dependent on a neural mechanism nor the release of neurotransmitters, but linked to translocation of calcium. It was reduced by incubation in Ca2+-free solution. Blockage of the Ca2+-ATPase pump, which inhibits the extrusion of calcium, plays a significant role in the process and enhances CIC. Cooling of gastrointestinal smooth muscle preparations induces graded myogenic contractions inversely proportional to the temperature. The mechanism is not dependent on local nervous control but related to a temperature-sensitive process of calcium translocation.

Animals↗
PubMed1991

Structure-activity relationships of rat neuromedin U for smooth muscle contraction.

Rat neuromedin U (r-NMU) and its fragment peptide amides were synthesized by solid-phase methodology. Using a chicken crop smooth muscle contraction assay, the potency of r-NMU and its fragments relative to porcine neuromedin U-8 (p-NMU-8) was r-NMU: 10.25 +/- 2.88, r-NMU (6-23): 8.01 +/- 1.04, r-NMU (10-23): 2.76 +/- 0.46, r-NMU (13-23): 2.81 +/- 0.52, and r-NMU (16-23): 0.88 +/- 0.19, respectively. Two heptapeptides, r-NMU (17-23) and r-NMU (16-22), had a relative potency of 0.61 and 0.03 respectively, and elicited maximal contraction at a dose of 10 microM to a similar degree to p-NMU-8. The other shorter C-terminal fragments did not elicit the maximal contraction or any activity. In a rat uterus contraction assay, r-NMU (13-23), but not r-NMU (16-23), at a dose of 4 nM retained as high a stimulatory activity as r-NMU itself. r-NMU (17-22) was the smallest peptide fragment to elicit the maximal sustained contraction at 10 microM. These results indicate that the amino acid sequence Phe-Leu-Phe-Arg-Pro-Arg, corresponding to positions 17 to 22 of r-NMU, may be essential for contractile activity. N-terminal peptide segments Tyr-Gln-Gly-Pro corresponding to positions 6 to 9, and Ser-Gly-Gly corresponding to positions 13 to 15, appear to be of special importance for potent activity.

Amino Acid Sequence↗
PubMed1991

Characteristics of tetanic muscle contraction in Parkinson patients.

The aim of this study was to examine contraction characteristics in striated muscles from Parkinson patients and to measure any changes in characteristics based on changes in medication. Fifteen patients, 9 men and 6 women, mean age 61.6 (range 43-70) with mild to moderate parkinsonism, (Hoehn and Yahr I-III) were investigated, and the results were compared with a group of 8 normal controls (mean age 59.6, range 50-70). Twelve of the patients (7 men and 5 women) were also tested after a 24-h period without medication. Using supramaximal electrical stimulation of the ulnary nerve at the wrist contraction, characteristics in the m. adductor pollicis muscle can be recorded. Stimulation results were printed on a fast paper writer. The following characteristics were recorded: 1) electromechanical delay of contraction EMDc; 2) contraction time to half tetanus CTT1/2; 3) electromechanical delay of relaxation EMDr; 4) relaxation rate RR for 10 ms RR-10; 5) the force produced in the tetanic contraction at stimulus frequencies 5, 10, 20, 50 Hz. The results showed that the in initiation of contraction (EMDc) was normal compared with controls. CTT1/2 was shorter (p less than 0.001) in the group of Parkinson patients compared with normals. EMDr was not changed when compared with normals, but RR-10 was increased, p less than 0.05. Force levels at the different stimulation rates were not significantly changed. After withdrawal of medication all parameters were unchanged. Muscle contraction characteristics in tetanic contraction were found to be abnormal indicating either a possible preactivation in the muscle contraction or a secondary change in the muscles of patients with Parkinson's disease.

Adult↗
PubMed1981

A comparison of frontal EMG biofeedback and neck EMG biofeedback in the treatment of muscle-contraction headache.

EMG biofeedback from the frontal area (FFB) was compared to EMG biofeedback from the neck (NFB) in the treatment of chronic muscle-contraction headache. Both treatment groups (N = 10) evidenced significant decreases in reported headache activity, with the NFB group also significantly reducing medication consumption. An analysis of EMG changes suggested that subjects were able to produce large within-session changes in EMG activity during initial sessions, with the major effect of additional training being an increase in speed with which these changes occurred. In neither group, however, did changes in EMG activity correspond closely to changes in reported headache activity.

Adolescent↗
PubMed2001

Effect of levator ani muscle contraction on urethrovesical and anorectal pressures and role of the muscle in urination and defecation.

OBJECTIVES: To investigate the effect of levator ani muscle (LAM) (the main muscle in the pelvic floor) contraction on the anorectal and urethrovesical pressures and elucidate its role in the mechanisms of defecation and urination. METHODS: In 18 healthy volunteers (10 men and 8 women; mean age 38.6 +/- 10.2 years), the LAM was stimulated to contract by a concentric needle electrode, and the anal, rectal, urethral, and vesical pressure responses were recorded. The test was repeated once after LAM anesthetization with Xylocaine injection and again after saline instead of Xylocaine injection into the LAM. RESULTS: On LAM stimulation, the anal and urethral pressures had a significant decline (both P <0.05), and the rectal and vesical pressures exhibited no significant changes (both P >0.05). The anal, rectal, urethral, and vesical pressures did not show significant changes on stimulation of the anesthetized LAM; after saline injection, the pressure response was similar to that before injection (P >0.05). These results were reproducible. CONCLUSIONS: LAM contraction lowers the anal and urethral pressures and appears to assist in the evacuation process. We therefore propose that the LAM is a muscle of evacuation and that LAM dysfunction could lead to defecation and urination disorders.

Adolescent↗
PubMed1997

Role of N-terminal active sites of galanin in neurally evoked circular muscle contractions in the guinea-pig ileum.

Synthetic galanin-related peptides and several galanin-(1-15)ol analogs were used to examine structure-function relationships of the N-terminal active site of galanin in more detail, using the guinea-pig ileum. The synthetic peptides examined showed their inhibitory activity on the neurally evoked circular muscle contractions with the following order of potency: rat, human and tuna galanin, galanin-(1-15)ol and [D-Trp8]galanin-(1-15)ol > N alpha-acetylated galanin-(2-15)ol, [Ala6,D-Trp8]galanin-(1-15)ol, galanin-(1-15) > tuna galanin-(1-15), [D-Ala8]galanin-(1-15)ol, N alpha-acetylated galanin-(1-15)ol. In contrast, [D-Thr6]galanin-(1-15)ol, [D-Tyr9]galanin-(1-15)ol and [D-Trp9]galanin-(1-15)ol were ineffective and showed no antagonistic activities to galanin. These results suggest that the L-configuration at positions 6 and 9 seems to be important for the inhibitory action of galanin on the neurally evoked guinea-pig circular muscle contractions.

Amino Acid Sequence↗
PubMed1991

Possible role of protein kinase C-dependent smooth muscle contraction in the pathogenesis of chronic cerebral vasospasm.

In the present study, we investigate the possible role of protein kinase C (PKC)-dependent smooth muscle contraction in cerebral vasospasm following subarachnoid hemorrhage (SAH), employing the beagle "two-hemorrhage" model. The occurrence of chronic vasospasm was angiographically confirmed on day 7 in the basilar artery, which was exposed via the transclival approach. The artery was superfused with aerated Krebs-Henseleit solution containing various agents, and the subsequent changes in the basilar artery diameter were recorded by successive angiography. The preexisting spasm was not ameliorated by local application of neurotransmitter antagonists (atropine, methysergide, phentolamine, and diphenhydramine), calmodulin inhibitors (R24571 and W-7), or a calcium antagonist, nicardipine. However, the application of PKC inhibitors such as H-7 and staurosporine induced significant dilation of the artery. In another experiment, an intrinsic PKC activator, 1,2-diacylglycerol (DAG), in the basilar artery, the CSF, and the cisternal clot of beagles exposed to two hemorrhages was measured on days 1, 2, 4, 7, and 14 using the DAG kinase method. On days 2, 4, and 7, the DAG content of the basilar artery showed a significant and prolonged increase (150-190% of control), whereas it was unchanged on days 1 and 14. Throughout the experimental period, there was a significant linear correlation between the DAG content and the angiographical diameter of the basilar artery. The above results indicate that SAH leads to an increase in the DAG level within the cerebral artery through an as yet unknown mechanism and that subsequent activation of the PKC-dependent contractile system participates in the occurrence of chronic vasospasm.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗
PubMed2005

Loss of ryanodine receptor calcium-release channel expression associated with overactive urinary bladder smooth muscle contractions in a detrusor instability model.

OBJECTIVE: To investigate the changes in spontaneous bladder smooth muscle contractions that occur during detrusor instability (DI), and to test the possibility that altered function or expression of ryanodine receptors (RyRs) could account for the increased bladder contractions. MATERIALS AND METHODS: After 8 weeks of partial bladder outlet obstruction, DI was confirmed in female experimental rats by filling cystometry. Muscle strips were dissected from freshly isolated bladders, and isometric tension recorded in strips from DI and normal bladders. The contractions were recorded during electrical stimulation or exposure to various agents. Western blot analysis was used to determine RyR expression in DI and normal bladder muscle. RESULTS: In DI bladder muscle, spontaneous contractile activity persisted in the presence of blockers for known neurotransmitter receptors in the bladder wall. The RyR blocker ryanodine significantly increased the spontaneous contractile frequency in normal bladder strips, but failed to affect spontaneous contractions in DI muscle. Caffeine inhibited spontaneous contractile activity in both the DI and normal strips. After administering the l-type Ca(2+) channel antagonist nimodipine, the myogenic contractile activity was abolished in normal strips; in contrast, in DI strips, the amplitude of contractions was reduced but the frequency of contractions was unchanged. Western blot analysis showed that RyR expression was lower in DI muscle than in normal bladder muscle. CONCLUSION: These results provide the first characterization of a loss of regulation of spontaneous contractile activity by RyRs in DI muscle associated with a significant decrease in RyR expression. RyRs in normal detrusor muscle act as negative-feedback regulators of spontaneous contractile activity, presumably by releasing Ca(2+) that activates Ca(2+)-dependent K(+) channels to decrease contractility. This mechanism might be weakened in DI muscle, resulting in spontaneous contractile overactivity.

Animals↗
PubMed2006

SmyD1, a histone methyltransferase, is required for myofibril organization and muscle contraction in zebrafish embryos.

Histone modification has emerged as a fundamental mechanism for control of gene expression and cell differentiation. Recent studies suggest that SmyD1, a novo SET domain-containing protein, may play a critical role in cardiac muscle differentiation. However, its role in skeletal muscle development and its mechanism of actions remains elusive. Here we report that SmyD1a and SmyD1b, generated by alternative splicing of SmyD1 gene, are histone methyltransferases that play a key role in skeletal and cardiac muscle contraction. SmyD1a and SmyD1b are specifically expressed in skeletal and cardiac muscles of zebrafish embryos. Knockdown of SmyD1a and SmyD1b expression by morpholino antisense oligos resulted in malfunction of skeletal and cardiac muscles. The SmyD1 morphant embryos (embryos injected with morpholino oligos) could not swim and had no heartbeat. Myofibril organization in the morphant embryos was severely disrupted. The affected myofibers appeared as immature fibers with centrally located nuclei. Together, these data indicate that SmyD1a and SmyD1b are histone methyltransferases and play a critical role in myofibril organization during myofiber maturation.

Alternative Splicing↗