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PubMed2004

The response of muscle interstitial F2-isoprostane (8-ISO-PGF2alpha) during dynamic muscle contractions in humans.

8-Iso-prostaglandin F2alpha (8-iso-PGF2alpha) is a characteristic F2-isoprostane which is produced in humans via a free radical-catalysed lipid peroxidation mechanism of arachidonic acid, independent of the cycloxygenase pathway. The measurement of the plasma levels of 8-iso-PGF2alpha was shown to be the most reliable biochemical index of oxidant stress status in the human body. However, there is no reference in literature of local muscle interstitial 8-iso-PGF2alpha production during dynamic muscle contractions. The aim of the present study was to evaluate the response of 8-iso-PGF2alpha during intensive exercise with a cycle ergometer. Two microdialysis probes with CMA-60 microdialysis catheters were inserted into the vastus lateralis muscle of the right leg of six healthy male volunteers. After insertion, these microdialysis probes were attached to a perfusion pump that perfused ringer acetate solution at a rate of 0.3 microl/min. The dialysate fluid samples were collected: (a) during a 30 min rest period and (b) during a 30 min period of dynamic exercise with a cycle ergometer at 150 Watts. Our measurements showed that the levels of 8-iso-PGF2alpha in the interstitial fluid (IF) of the vastus lateralis muscle increase significantly during exercise (from 113.5 +/- 30.2 to 329.9 +/- 69.8 pg/ml, P = 0.05). In conclusion, dynamic muscle exercise produces a local increase of the IF levels of 8-iso-PGF2alpha due to local peroxidation injury of the contractive muscle. The microdialysis method is widely applied, easily repeated and it could contribute in evaluating the local lipid muscle peroxidation during intensive exercise.

Adult↗

PubMed1993

Expression of bombesin-receptor subtypes and their differential regulation of colonic smooth muscle contraction.

BACKGROUND: Bombesin-related peptides show different potencies, suggesting the existence of at least two receptor subtypes. The aim of this study was to assess the relationship and contribution of each receptor subtype on smooth muscle contraction. METHODS: The expression of bombesin-receptor subtype messenger RNA (mRNA) was examined in human and rabbit smooth muscle from the rectosigmoid colon, and the contribution of each of the receptor subtypes to smooth muscle contraction was investigated by blocking mRNA translation of either neuromedin B or gastrin-releasing peptide (GRP) receptor subtype or of both. RESULTS: Neuromedin B and GRP receptor mRNAs were detected in human and rabbit colonic smooth muscle cells. Incubation with neuromedin B receptor antisense oligonucleotides inhibited the neuromedin B-induced contraction, whereas incubation with GRP receptor antisense oligonucleotides inhibited the GRP-induced contraction. Incubation with GRP plus neuromedin B receptor antisense oligonucleotides inhibited the contractile response induced by bombesin, neuromedin B, and GRP. CONCLUSIONS: Distinct neuromedin B and GRP receptor subtypes are present on smooth muscle cells of the rectosigmoid colon, and bombesin interacts with both neuromedin B and GRP receptors, resulting in a complex contraction that is sustained in nature.

Animals↗

PubMed1976

Release of smooth muscle-contracting substances from isolated perfused lungs.

Infusion of tryptamine (1-4 mug/ml) through the pulmonary circulation of rat isolated lung perfused with Krebs solution caused release of a mixture of spasmogens contracting isolated smooth muscle preparations. One component of this mixture had biological activity comparable to E-type prostaglandins. Other components included a slow reacting substance comparable to SRS-A and a rabbit aorta-contracting substance comparable to RCS. Infusions of 5-hydroxytryptamine, acetylcholine and histamine (0.5-2 mug/ml) also caused release. Release induced by the tryptamines but not that by acetylcholine and histamine was prevented by methysergide whereas acetylcholine-induced release was prevented by hyoscine which did not affect tryptamine-induced release. The tryptamines and histamine released spasmogens from dog isolated lungs but only histamine was effective in guinea-pig lungs. We conclude that amine-induced release from isolated lungs is a fairly general phenomenon and that it may represent an endocrine function of lung.

Acetylcholine↗

PubMed2003

Evaluation of indices of skeletal muscle contraction in areas of referred hyperalgesia from an artificial ureteric stone in rats.

This study examined indices of skeletal muscle contraction in a rat model of referred muscle hyperalgesia from artificial ureteric calculosis [left oblique muscle (OE) for ipsilateral stone]. In specimens from the left versus right OE of stone-implanted female rats, a significant increase was found in membrane fluidity (P<0.01) and Ca(2+)-ATPase activity (P<0.0001) and a significant decrease in 3H-ryanodine binding (P<0.0001) and in I band length/sarcomere length ratio (contraction index) (P<0.01). The increase in Ca(2+)-ATPase activity was directly and significantly related to the number of rats' ureteral 'crises' (P<0.02). The results indicate a state of contraction in the hyperalgesic muscle, whose extent correlates to the algogenic activity of the ureteral stone.

Animals↗

PubMed1983

The relationship between tegumental disruption and muscle contraction in Schistosoma mansoni exposed to various compounds.

The antischistosomal drugs praziquantel and Ro 11-3128, which cause a tetanic contraction of Schistosoma musculature, concurrently produce a disruption of the parasite's tegument. Both phenomena are attenuated by preincubation of the parasites in high Mg2+ containing media before addition of the drugs, and the therapeutically inactive stereoisomers of these drugs cause neither effect. Other antischistosomal drugs tested cause neither muscle contraction nor tegumental disruption. Some unrelated agents which cause muscle contraction (but have no antischistosomal effect) alter the parasite's tegument, while others do not. Cytochalasin B, but not colchicine, causes tegumental disruption without affecting muscle tension. Thus, there is no simple correlation between a drug's antischistosomal activity or ability to contract the parasite's muscle and its ability to damage the parasite's tegument.

Animals↗

PubMed1989

[The mechanism of ergonovine-induced airway smooth muscle contraction].

There have been three articles in the clinical literature concerning ergonovine maleate-induced bronchospasm. The effect of this alkaloid on isolated canine tracheobronchial smooth muscle was analyzed to investigate the mechanism of ergonovine-induced airway smooth muscle contraction. Both ergonovine and serotonin (5-hydroxytryptamine, 5HT) contracted canine tracheal smooth muscle with EC50 1.4 X 10(-8) M and 5.1 X 10(-7) M, respectively. The maximal contractile response observed with ergonovine was approximately 30% less than that observed with 5HT. In diverse blockers such as methysergide, atropine, prazosin, propranolol, pyrilamine and cimetidine, only methysergide competitively blocked both ergonovine and 5HT responses with a similar calculated dissociation constant (pKB); 8.3 +/- 0.2 against ergonovine and 8.5 +/- 0.2 against 5HT (n = 6, p = 0.9). The relative affinity and efficacy of ergonovine and 5HT were determined by use of a partial irreversible antagonist, phenoxybenzamine. The calculated affinity of ergonovine was about 16 times higher than that of 5HT. The relative efficacy of EC100 for ergonovine was 0.2 but at EC10 it was 41.9 (5HT efficacy = 1). Ergonovine 10(-9) M or 10(-8) M shifted the 5HT dose-response curve to the right without reducing the maximal response, but the shift was nonparallel. Ergonovine and 5HT also contracted canine bronchial smooth muscle in a dose dependent manner with EC50 6.4 X 10(-8) M and 1.8 X 10(-7) M, respectively. The dose-responses curve of these two agonists were competitively blocked by methysergide 10(-6) M. These data indicate that ergonovine directly contracts canine tracheobronchial smooth muscle as a result of its combination with 5HT receptors. This effect may result in the precipitation of an asthmatic attack in susceptible individuals.

Animals↗

PubMed2003

Increase in endothelial cell Ca(2+) in response to mouse cremaster muscle contraction.

We addressed the role of endothelial cells (ECs) in metabolic dilatation of skeletal muscle arterioles in anaesthetized mice in situ. Electrical field stimulation was used to contract the cremaster muscle for 15 s at 30 Hz. Diameter was observed using bright field microscopy. In controls, muscle contraction produced a 15.7 +/- 1.5 microm dilatation from a baseline of 17.4 +/- 1.6 microm. Endothelial denudation (-EC) via intraluminal perfusion of air abolished this response (1.6 +/- 1.2 microm in -EC, P < 0.05), identifying endothelium as the primary vascular cell type initiating the dilatation. To investigate the role of EC Ca(2+) in metabolic dilatation, arteriolar ECs were loaded with Fluo-4 AM or BAPTA AM by intraluminal perfusion, after which blood flow was re-established. Ca(2+) activity of individual ECs was monitored as a function of change from baseline fluorescence using confocal microscopy. In ECs, whole cell Ca(2+) increased (>10%, P < 0.05) during muscle contraction, and localized Ca(2+) transients were increased (>20%, P < 0.05) during the first minute after contraction. Chelation of EC Ca(2+) abolished the dilatations in response to muscle contraction (1.1 +/- 0.7 microm, P < 0.05). Inhibition of P(1) purinergic receptors (with xanthine amine congener) did not alter the rate of onset of the dilatation (P > 0.05) but decreased its magnitude immediately post stimulation (7.1 +/- 0.9 microm, P < 0.05) and during recovery. These findings demonstrate obligatory roles for endothelium and EC Ca(2+) during metabolic dilatation in intact arterioles. Furthermore, they suggest that at least two separate pathways mediate the local response, one of which involves stimulation of endothelial P(1) purinergic receptors via endogenous adenosine produced during muscle activity.

Adenosine↗

PubMed1986

High voltage versus low voltage electrical stimulation. Force of induced muscle contraction and perceived discomfort in healthy subjects.

High voltage pulsed galvanic stimulation (HVPGS) and low voltage neuromuscular stimulation (LVNMS) techniques were compared for peak torque of an induced isometric contraction, perceived discomfort, and subjective preference of treatment. The high voltage current used a 40-microseconds monophasic waveform, and the low voltage current used a 300-microseconds biphasic waveform. Both currents used a pulse rate of 50 pps. Both HVPGS and LVNMS were administered to one muscle group, either knee extensors or plantar flexors, of 24 healthy subjects. An isokinetic dynamometer was used to assess peak torque. The perceived discomfort experienced with each type of electrical stimulation was quantified by the use of a visual analog scale. For all dependent measures, data first were analyzed for the whole treatment group and then analyzed for each subgroup. Correlated t tests for the whole group and the plantar flexor muscle subgroup demonstrated that HVPGS produced a significantly greater average peak force of muscle contraction than LVNMS and HVPGS was perceived to be significantly less uncomfortable than LVNMS. No significant differences were found between treatments in the knee extensor muscle subgroup for these dependent variables. Chi-square analysis revealed a subject preference for HVPGS in the whole group and in both subgroups. This study indicates that HVPGS can produce a stronger, less uncomfortable, induced isometric muscle contraction than LVNMS.

Consumer Behavior↗

PubMed2000

Influence of microtubules on vascular smooth muscle contraction.

Microtubules are ubiquitous in eukaryotic cells and play key roles in many cellular activities. The purpose of this study was to investigate the influence of microtubules on vascular smooth muscle contraction. Quantitative immunocytochemical analysis of rat aortic tissue revealed that, relative to the control group, colchicine (15 muM, 90 min) and nocodazole (15 muM, 90 min) decreased the microtubule density by 40-50% while taxol (10 muM, 90 min) increased the microtubule density by 33%. Isometric contraction studies demonstrated that both colchicine and nocodazole caused an upward shift in the phenylephrine (10(-8) to 10(-5) M) dose-response curve while taxol caused no significant change when compared to the control group. Potassium chloride (30 mM) induced 55 +/- 5% P0 contraction in DMSO treated vessel rings. The active tension increased to 73 +/- 5% P0 and 71 +/- 6% P0 after pretreatment of the aortic rings with colchicine or nocodazole, respectively. Taxol did not cause a significant change in the active tension (56 +/- 7% P0). These results indicate that microtubule depolymerization enhances isometric contraction of vascular smooth muscle and this enhanced contraction is not receptor dependent. Pretreatment of the aortic rings with an inhibitor of nitric oxide synthase (NOS) (Nomega-nitro-L-arginine) did not change the increased contractile response to phenylephrine due to microtubule depolymerization suggesting that this phenomenon is not mediated by endothelium dependent relaxation.

Animals↗

PubMed1993

Ras proteins increase Ca(2+)-responsiveness of smooth muscle contraction.

G-proteins may be involved in receptor-mediated Ca(2+)-sensitization of smooth muscle contraction, but the responsible G-proteins are not yet known. Here we show that in beta-escin skinned mesenteric microarteries, H-ras p21 proteins, preactivated with GTP or GTP gamma S, increase force at constant submaximal Ca2+ (pCa 6.3) concentration dependently. The GTP-bound form of the wild-type H-ras p21 and the oncogenic mutant (p21[G12V]) were equally effective. The nucleotide-free and the inactive GDP-bound form of ras p21 had no effect on force. The tryosine kinase inhibitor, tryphostin, partially reversed the effect of the ras proteins in the GTP-bound form on force. Thus, ras proteins mimic the Ca(2+)-sensitizing effect of GTP gamma S and vasoconstrictors in mesenteric microarteries which may involve tyrosine phosphorylation.

Animals↗

PubMed1999

Pressor reflex evoked by static muscle contraction: role of nitric oxide in the dorsal horn.

In this study, we tested the hypothesis that nitric oxide (NO) production in the dorsal horn is involved in producing the pressor reflex elicited by static contraction of skeletal muscle. Cats were anesthetized with alpha-chloralose (80 mg/kg) and urethane (100 mg/kg), and a laminectomy was performed. With the exception of the L7 dorsal root, the dorsal and ventral roots from L5 to S2 were sectioned on one side and static contraction of the ipsilateral triceps surae muscle was evoked by electrically stimulating the peripheral ends of the L7 and S1 ventral roots. Dialysis of the NO synthase inhibitor NG-nitro-L-arginine methyl ester (L-NAME; 50 mmol/l syringe concentration, based upon dose-response data) into the dorsal horn at L6 and S1 failed to attenuate the peak change in mean arterial pressure (MAP) evoked by static contraction (DeltaMAP in mmHg: 57 +/- 5 before and 50 +/- 6 after 2 h of L-NAME). However, this dialysis of L-NAME reduced the magnitude of the initial pressor response as the MAP at 10 s of the contraction fell from 27 +/- 4 to 17 +/- 4 mmHg. On the other hand, 2 h of L-arginine dialysis (50 mmol/l) shifted the curve representing the time course of the pressor response upward and increased the peak pressor response to static contraction from 51 +/- 9 to 68 +/- 9 mmHg. A 2-h dialysis of D-NAME (50 mmol/l), the inactive enantiomer of L-NAME, had no effect on the time course or the peak pressor response (DeltaMAP in mmHg: 78 +/- 12 before and 72 +/- 15 after). These data suggest that NO production in the dorsal horn has a modulatory influence on the pressor reflex evoked by static contraction of skeletal muscle and that increasing the level of NO in the dorsal horn enhances the excitability of dorsal horn cells to muscle afferent input.

Animals↗

PubMed1995

Dependency of upper airway patency on head position: the effect of muscle contraction.

In the present study we examined the effect of flexion and extension of the head on upper airway (UAW) patency in anesthetized dogs, and compared the dilatory and stabilizing effects of electrically stimulated UAW muscles at the different head positions. Flexion of the head increased UAW resistance (Ruaw) and reduced maximal flow (Vmax), but had little effect on the negative pressure at which UAW collapse occurred (Pcrit). Extension of the head, on the other hand, resulted in more negative Pcrit values and increased Vmax without significantly affecting Ruaw. Electrically induced UAW muscle contraction affected the pressure-flow curve and Ruaw, as well as Pcrit. Changing head position had a substantial effect on the dilatory and stabilizing effect of the various UAW muscles. However, independent of head position, genioglossus stimulation was most effective in reducing Ruaw and increasing Pcrit. We conclude that in the anesthetized, supine dog, head position affects the mechanical properties of the UAW and the effects of UAW muscle contraction.

Airway Resistance↗

PubMed1969

A proposed common allosteric mechanism for active transport, muscle contraction, and ribosomal translocation.

It is suggested that active transport, muscle contraction, and ribosomal translocation may all make use of a common allosteric mechanism in which ATP or GTP serves as both the effector and substrate and in which a conformational change in a protein (enzyme) moves or exerts a force on a second ligand. The enzymatic splitting of ATP or GTP provides the driving force for the process and allows repetition of the steady-state cycle.

Adenosine Triphosphate↗

PubMed2002

Kinetic effects of myosin regulatory light chain phosphorylation on skeletal muscle contraction.

Kinetic analysis of contracting fast and slow rabbit muscle fibers in the presence of the tension inhibitor 2,3-butanedione monoxime suggests that regulatory light chain (RLC) phosphorylation up-regulates the flux of weakly attached cross-bridges entering the contractile cycle by increasing the actin-catalyzed release of phosphate from myosin. This step appears to be separate from earlier Ca(2+) regulated steps. Small step-stretches of single skinned fibers were used to study the effect of phosphorylation on fiber mechanics. Subdivision of the resultant tension transients into the Huxley-Simmons phases 1, 2(fast), 2(slow), 3, and 4 reveals that phosphorylation reduces the normalized amplitude of the delayed rise in tension (stretch activation response) by decreasing the amplitudes of phase 3 and, to a lesser extent, phase 2(slow). In slow fibers, the RLC P1 isoform phosphorylates at least 4-fold faster than the P2 isoform, complicating the role of RLC phosphorylation in heart and slow muscle. We discuss the functional relevance of the regulation of stretch activation by RLC phosphorylation for cardiac and other oscillating muscles and speculate how the interaction of the two heads of myosin could account for the inverse effect of Ca(2+) levels on isometric tension and rate of force redevelopment (k(TR)).

Animals↗

PubMed1997

Effects of JTV-506, a new K+ channel activator, on airway smooth muscle contraction and systemic blood pressure.

BACKGROUND: ATP-sensitive K+ (KATP) channel activators produce relaxation of smooth muscle in many tissues. However, this wide range of effects restricts their clinical usefulness in bronchial asthma because of a reduction in systemic blood pressure. METHODS: We have now examined the effects of JTV-506, a new benzopyran derivative, on airway smooth muscle contraction and systemic blood pressure and have compared this compound with cromakalim. We measured isometric tension records from guinea-pig isolated trachea, as well as the respiratory resistance (Rrs) and systemic blood pressure in anesthetized guinea-pigs. RESULTS: JTV-506 caused a concentration-dependent inhibition of histamine-induced contraction in guinea-pig isolated tracheal smooth muscle, and was antagonized by glibenclamide. JTV-506 was 7.6-fold more potent than cromakalim. In anesthetized animals the intravenous injection of JTV-506 reduced the increase in Rrs induced by intravenous application of 5 micrograms/kg of histamine in a dose-dependent manner. 10 micrograms/kg of JTV-506 resulted in 57.0 +/- 17.9% inhibition of the increase in Rrs at 10 min. The inhibitory action on Rrs disappeared after 60 min. 10 micrograms/kg of cromakalim caused 25.4 +/- 5.8% inhibition of the increase in Rrs induced by histamine at 1 min. The ED50 values for JTV-506 and cromakalim were 6.7 +/- 3.5 micrograms/kg and 60.1 +/- 15.8 micrograms/kg, respectively (P < 0.05). Cromakalim was approximately 9-fold less potent in inhibiting the increased Rrs by histamine, and the inhibitory action lasted less than 10 min. The reduction of systemic blood pressure by JTV-506 and cromakalim (each at a dose of 10 micrograms/kg iv) was 11.3% and 21.5%, respectively (P < 0.05). CONCLUSION: JTV-506 inhibits histamine-induced contraction of tracheal smooth muscle by activation of KATP channels. This compound is more potent and longer-lasting in the suppression of histamine-induced increases in Rrs, and is less hypotensive than cromakalim. Our results suggest that this compound merits further investigation for utility as a bronchodilator in the clinic.

Animals↗

PubMed1985

alpha-Adrenoceptor agonists and the Ca2+-dependence of smooth muscle contraction: evidence for subtypes of receptors or for agonist-dependent differences in the agonist-receptor interaction?

The effects of varying [Ca2+]o on the contraction of smooth muscle by different alpha-adrenoceptor agonists were examined on rat isolated anococcygeus muscle. Agonists were tested in the presence of various [Ca2+]o or 'Ca2+-re-addition curves' were constructed. In some experiments the [Ca2+]free was buffered with EGTA and nitrilotriacetic acid. The components of the response which were revealed were further analysed by using drugs which modify Ca2+ mobilization. Three separate elements in the contractile response were identified: (i) an initial transient contraction, due to intracellular Ca2+ release could be isolated with [Ca2+]o between 1 nmol/l and 3 mumol/l (this could be obtained only with noradrenaline, phenylephrine and amidephrine); (ii) a nifedipine-sensitive response requiring [Ca2+]o of 3 mumol/l or more; (iii) a nifedipine-resistant response requiring [Ca2+]o of 100 mumol/l or more. Presumably (ii) and (iii) involve the entry of Ca2+o: they could be obtained with all agonists tested, including these above, methoxamine, indanidine and xylazine. The results are discussed in relation to the possibility of distinct types of response and their relationship to subgroups of receptors or agonists. It is concluded that there is a continuous spectrum of activity across the agonist range and that this is likely to correlate with 'efficacy' at a single alpha 1 receptor type.

Adrenergic alpha-Agonists↗

PubMed1988

Roles of CO2, O2, and acid in arteriovenous [H+] difference during muscle contractions.

To determine the origins of the arteriovenous [H+] difference of muscle during contractions, arterial and muscle venous blood sample pairs were taken before and after 0.5, 5.0, and 30.0 min of 4/s isometric twitches of the gastrocnemius-plantaris muscle group of anesthetized dogs. These samples were analyzed for PO2, PCO2, and pH, the concentrations of O2, CO2, K+, Na+, La-, and Cl- in whole blood, and La-, K+, Na+, and Cl- in plasma. Whole blood was hemolyzed and analyzed for PO2, PCO2, and pH. Net O2 uptake, CO2 output, L, K+, Na+, and Cl- were calculated in addition to net output of non-CO2 acid (HA) and strong ion difference ([SID]) and common ion [SID] ([K+] + [Na+] - [Cl-] - [La-]). From these data we partitioned the origins of the arteriovenous [H+] difference via the common PCO2-pH diagram and via a [H+]-PCO2 diagram and determined whether true plasma arteriovenous [H+] differences reflect plasma and cell arteriovenous [H+] differences. The arteriovenous [H+] differences of plasma and hemolyzed blood were the same, showing that true plasma does reflect plasma and cells. K+ showed a small significant but transient output. Na+ was not significant, whereas Cl- showed a significant transient uptake. Lactate output and HA, calculated for dog blood acid-base, showed transient outputs and were the same. At 5.0 min when the arteriovenous difference was largest, CO2 alone would have increased [H+] 15.9 nmol/l whereas desaturation of Hb would have decreased [H+] 4.2 nmol/l and lactate could have raised [H+] 1.0 nmol/l.(ABSTRACT TRUNCATED AT 250 WORDS)

Acid-Base Equilibrium↗

PubMed1989

[Occurrence of muscle contraction headache in children with abnormal incisor occlusion].

The principal result of the investigation indicates that children with abnormal incisor occlusion must be regarded as a risk group concerning muscle contraction headache (MCH). The need for orthodontic treatment of children with abnormal incisor occlusion is usually by layman regarded as being based upon psychosocial considerations. These considerations shall not be underestimated. For children as well as for grown up persons an appearance dominated by a visible abnormal incisor occlusion will be loading in contact with other people. From a professional point of view need for orthodontic treatment of children with abnormal incisor occlusion has usually been defined from the demand for stability. Grown up people with abnormal incisor relations are frequently referred to orthodontic specialists because of problems, such as migration of the incisors, extreme attrition or functional disturbances in the masticatory system. These problems are closely related to the abnormal incisor occlusion. With our present knowledge of the importance of the incisor relation for the function of the masticatory system, this condition must have high priority in the evaluation of need for orthodontic treatment of children. The treatment will, by improving the functional condition of the masticatory system and normalizing the function, have importance as prophylaxis and/or early treatment of a risk group concerning muscle contraction headache.

Child↗