PubMed Health⌕ Search

SEARCH · PubMed Health

Results for “Muscle Contraction”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 1,729 records · Page 96Linked to original sources
PubMed1990

Endotoxin-induced impairment of vascular smooth muscle contractions elicited by different mechanisms.

The current study was designed to analyse the mechanisms which are impaired in the vascular hyporeactivity to contractile agents induced by E. coli lipopolysaccharide endotoxin (LPS). Endothelium-denuded aortic rings were prepared from thoracic aorta removed from control and LPS-pretreated rats (20 mg/kg i.p., 4 h before the experiment). In order to determine whether LPS treatment altered the contractile components that depend on intracellular calcium release and extracellular calcium entry to the same extent, rings were contracted under various experimental conditions. The responses elicited by indanidine, phenylephrine (without and with nitrendipine 1 microM), (-) Bay K 8644, (+) S 202-791 and the calcium ionophore calimycin in the presence of 1.25 mM external CaCl2 were all impaired by LPS pretreatment (maximal contractions 19, 63, 44, 28, 22 and 22% of controls, respectively). Concentration-effect curves for CaCl2 made in depolarizing medium (KCl 40 and 100 mM) and in the presence of calimycin (3 microM) were shifted to the right in rings from LPS-pretreated rats. However, the LPS-induced depression of contraction was overcome by the addition of CaCl2 (up to 30 mM). Additionally, in the absence of external CaCl2, the contraction induced by caffeine (50 mM) was not significantly altered by LPS treatment. It is concluded that LPS treatment does not reduce the ability of aortic smooth muscle cells to contract. The results suggest that LPS treatment impairs mechanisms involved in calcium handling within smooth muscle cells after stimulation of calcium entry through different pathways and activation of intracellular calcium release by alpha 1-adrenoceptor agonists.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMed1988

Arteriolar diameter and tissue oxygen tension during muscle contraction in hypertensive rats.

This study evaluated the possibility that in hypertension, mechanisms that maintain near normal arteriolar diameters at elevated arteriolar pressures limit the ability of skeletal muscle arterioles to dilate in response to an increase in tissue metabolism. The spinotrapezius muscles of 16- to 20-week-old spontaneously hypertensive rats (SHR) and Wistar-Kyoto rats (WKY) were contracted at frequencies of 1, 2, 4, and 8 Hz. The inner diameters of first-order through third-order arterioles were measured at rest and following 3 minutes of contractions. Tissue oxygen tension (PO2) at the venous end of capillaries was monitored during 8-Hz contractions. At rest, following contractions, and after maximum dilation with adenosine, the inner diameters of arterioles of equivalent branch order were not significantly different in SHR and WKY. Opening of closed arterioles during muscle contraction and adenosine application occurred in less than 5% of the observations in both groups. The resting tissue PO2 was 25.5 +/- 1.3 mm Hg in normal rats and 26.1 +/- 2.1 mm Hg in SHR. At nearly maximum vasodilation during 8-Hz stimulation, tissue PO2 recovered to 81.9 +/- 12.7% of control in WKY but only to 41.2 +/- 13.0% of control in SHR. These observations indicate that the expression of local regulatory mechanisms related to tissue metabolism is virtually normal in the spinotrapezius muscle vasculature of SHR in the context of arteriolar dilation. However, at near maximum performance, factors other than absolute arteriolar diameter preclude the normal preservation of tissue PO2 in the spinotrapezius muscle of SHR.

Animals↗
PubMed1985

Energetic aspects of skeletal muscle contraction: implications of fiber types.

In this chapter fundamental energetic properties of skeletal muscles as elucidated from isolated muscle preparations are described. Implications of these intrinsic properties for the energetic characterization of different fiber types and for the understanding of locomotion have been considered. Emphasis was placed on the myriad of physical and chemical techniques that can be employed to understand muscle energetics and on the interrelationship of results from different techniques. The anaerobic initial processes which liberate energy during contraction and relaxation are discussed in detail. The high-energy phosphate (approximately P) utilized during contraction and relaxation can be distributed between actomyosin ATPase or cross-bridge cycling (70%) and the Ca2+ ATPase of the sacroplasmic reticulum (30%). Muscle shortening increases the rate of approximately P hydrolysis, and stretching a muscle during contraction suppresses the rate of approximately P hydrolysis. The economy of an isometric contraction is defined as the ratio of isometric mechanical response to energetic cost and is shown to be a fundamental intrinsic parameter describing muscle energetics. Economy of contraction varies across the animal kingdom by over three orders of magnitude and is different in different mammalian fiber types. In mammalian skeletal muscles differences in economy of contraction can be attributed mainly to differences in the specific actomyosin and Ca2+ ATPase of muscles. Furthermore, there is an inverse relationship between economy of contraction and maximum velocity of muscle shortening (Vmax) and maximum power output. This is a fundamental relationship. Muscles cannot be economical at developing and maintaining force and also exhibit rapid shortening. Interestingly, there appears to be a subtle system of unknown nature that modulates the Vmax and economy of contraction. Efficiency of a work-producing contraction is defined and contrasted to the economy of contraction. Unlike economy, maximum efficiency of work production varies little across the animal kingdom. There are difficulties associated with the measurement of maximum efficiency of contraction, and it has yet to be determined unequivocally if the maximum efficiency of contraction varies in different fiber types. The intrinsic properties of force per cross-sectional area, economy, and Vmax determine the basic energetic properties of skeletal muscles. Nonetheless, the mechanics and energetics of skeletal muscles in the body are profoundly influenced by muscle architecture, attachment of muscles to the skeleton, and motor unit organization.(ABSTRACT TRUNCATED AT 400 WORDS)

Actomyosin↗
PubMed1992

Depolarization of Ib afferent axons in the cat spinal cord during homonymous muscle contraction.

1. Intra-axonal records from the intraspinal course of Ib and Ia afferent fibres innervating the gastrocnemius medialis muscle were obtained in chloralose or Nembutal-anaesthetized cats during submaximal contractions of the muscle. 2. Afferent fibres in continuity with their muscle of origin were functionally identified by their responses to muscle stretch or contraction. 3. In six out of eight Ib afferents, primary depolarizations (PADs) were recorded during contraction. They were independent of the presence of orthodromic impulses fired by tendon organs. 4. These observations support the assumption that the reduction of Ib autogenetic inhibition in homonymous and synergic motoneurones during GM contractions is due to presynaptic inhibition of transmission in Ib pathways.

Animals↗
PubMed1982

Interaction of histamine with adrenergic smooth muscle neurotransmission. I. Effects of histamine on smooth muscle contractions induced by exogenous or by endogenous noradrenaline.

The effects of histamine on contractions in response to exogenous noradrenaline or to electrical stimulation were studied on two smooth muscle preparations with adrenergic neurotransmission--rat anococcygeal muscle and vas deferens. Histamine (1 X 10(-6)M-1 X 10(-4)M) did not affect significantly the contractions of vas deferens induced by noradrenaline (1 X 10(-8)M-1 X 10(-4)M), but decreased in a concentration-dependent manner the contractile effects of noradrenaline on anococcygeal muscle. The EC50 of noradrenaline on the latter preparation was increased 2.6-16.2 times by histamine but the antagonism was of a noncompetitive type. Histamine exerted a biphasic effect on the smooth muscle contractions in response to square wave electrical stimulation with supramaximal voltage (vas deferens--0.1 Hz, 1 sh or 10 Hz, 20 sh; anococcygeal muscle--5 Hz, 8 sh or 10 Hz 20 sh). The lower histamine concentrations (1 X 10(-12)M-1 X 10(-7)M) slightly potentiated the contractions and the higher concentrations (1 X 10(-6)M-1 X 10(-4)M) markedly inhibited the contractions in response to electrical stimulation. The results obtained are consistent with the hypothesis that the modulatory role of histamine for the adrenergic neurotransmission is mediated via presynaptic inhibitory H2--and postsynaptic excitatory H1--histaminergic receptors.

Animals↗
PubMed1990

Phorbol esters inhibit smooth muscle contractions through activation of Na(+)-K(+)-ATPase.

1. The role of protein kinase C (PKC) in agonist-induced contractions of guinea-pig ileum longitudinal smooth muscle has been investigated. 2. The phorbol esters, phorbol 12,13-dibutyrate (PDBu), phorbol 12,13-diacetate (PDA) and phorbol 12-myristate 13-acetate (PMA), relaxed tissues precontracted by submaximal concentrations of carbachol, histamine or substance P. 3. This inhibitory action of the phorbol esters was reversed following the application of ouabain, a specific inhibitor of Na(+)-K(+)-ATPase. Similarly, pretreatment with ouabain inhibited the ability of phorbol esters to relax tissues precontracted by the above agonists. 4. The slow relaxation of the tonic component of contraction induced by submaximal concentrations of carbachol and histamine, and all concentrations of substance P, was abolished in the presence of ouabain. 5. In Na(+)-loaded tissues, PDBu and carbachol caused a concentration-dependent increase of Na(+)-K(+)-ATPase activity, assessed by ouabain-sensitive 86Rb(+)-uptake. Extrusion of Na+, assessed by the cellular content of the ion, was also stimulated by PDBu (the effect of carbachol was not investigated). 6. We conclude that phorbol esters inhibit the tonic component of contractions induced by submaximal concentrations of these agonists through activation of Na(+)-K(+)-ATPase. We suggest that PKC may exert feedback control over the tonic component of agonist contractions through stimulation of the pump.

Animals↗
PubMed2002

Ozone exposure may enhance airway smooth muscle contraction by increasing Ca(2+) refilling of sarcoplasmic reticulum in guinea pig.

Ozone induces airway hyperresponsiveness, but there is controversy about effects of ozone on smooth muscle per se. We therefore investigated effects of in vivo ozone exposure on intracellular calcium mobilization in relation to tracheal smooth muscle contractility in the guinea pig in vitro. Guinea pigs underwent ozone exposure or sham exposure (3 ppm, 2 h). Then, a tracheal smooth muscle strip was mounted in an organ bath to record isometric tension. Effects of ozone exposure on acetylcholine-induced contraction of smooth muscle were as follows. Contraction was not altered in normal Krebs solution, but was increased in Ca(2+)-free solution in ozone-exposed animals. Decline of tension on repetitive application of acetylcholine in Ca(2+)-free solution was reduced, while the tension decline rate while acetylcholine was washed out with Ca(2+)-free solution was facilitated in ozone-exposed animals. Tension decline during the continuous administration of acetylcholine in Ca(2+)-free solution was slowed. Contraction occurred more quickly in Ca(2+)-free solution in ozone-exposed animals. Results suggest that ozone has a direct action on airway smooth muscle by changing Ca(2+) mobilization; Ca(2+) refilling via a Ca(2+) pump and Ca(2+) release via Ca(2+) channels in the sarcoplasmic reticulum were increased, while Ca(2+) extrusion via the plasma membrane Ca(2+) pump was unchanged.

Acetylcholine↗
PubMed1989

Inhibitory effect of lithium on muscle contractions caused by various stimulants in guinea-pig ileum.

The tonic contractions induced in the guinea-pig ileal longitudinal muscle by 60 mM KCl, carbachol, histamine or A23187 were inhibited similarly by Li+-substituted solution. There was a good correlation between the Li+-induced inhibition of contractions induced by these stimulants and the intracellularly accumulated Li+ content. In the experiment with fura-2, Li+-substituted solution inhibited the high-K+-induced contraction without decreasing the cytosolic Ca2+ level elevated by high-K+ solution. The concentration-response curve for Ca2+ in the skinned fiber was shifted to the right by pretreatment with Li+-substituted solution. These results suggest that the inhibitory mechanism of Li+ on the contractions by various stimulants partly involves the direct inhibition of the contractile proteins in the guinea-pig ileal longitudinal muscle.

Animals↗
PubMed1998

Nitric oxide relaxes bovine ciliary muscle contracted by carbachol through elevation of cyclic GMP.

It is generally accepted that nitric oxide relaxes vascular smooth muscles by activating guanylyl cyclase, which in turn increases cyclic 3':5' guanosine monophosphate level. Despite the physiological significance of nitric oxide, very few studies have attempted to characterize the mode of action of this mediator in ciliary muscles. Therefore, the present experiments were designed to investigate whether or not the relaxation induced by sodium nitroprusside as a donor of nitric oxide is accompanied by the increase in cyclic 3':5' guanosine monophosphate level in the bovine ciliary muscle, and these responses are affected by methylene blue as an inhibitor of guanylyl cyclase and 3-isobutyl-1-methylxanthine as an inhibitor of phosphodiesterases. The relaxation activity of exogenous 8-bromo-cyclic 3':5' guanosine monophosphate was also determined. Sodium nitroprusside produced a concentration-dependent relaxation in the bovine ciliary muscle strips which had been contracted by carbachol as a cholinergic agonist. Relaxation in response to sodium nitroprusside was accompanied by a significant (P<0.05 and P<0.005) increase in cyclic 3':5' guanosine monophosphate level. The relaxation response and the increase in cyclic 3':5' guanosine monophosphate caused by sodium nitroprusside were significantly (P<0.01 and P<0.05) augmented by the pretreatment with 3-isobutyl-1-methylxanthine, and were significantly (P<0.005 and P<0.05) attenuated in the presence of methylene blue. The exogenously applied 8-bromo-cyclic 3':5' guanosine monophosphate relaxed the ciliary muscle strips in a concentration-dependent manner. These results suggest that nitric oxide causes relaxation of the bovine ciliary muscle through the activation of guanylyl cyclase and an increase in cyclic 3':5' guanosine monophosphate level.

1-Methyl-3-isobutylxanthine↗
PubMed2006

Differences in exercising limb blood flow variability between cardiac and muscle contraction cycle related analysis during dynamic knee extensor.

AIM: Blood flow in peripheral conduit arteries during steady-state, dynamic exercise, can be estimated noninvasively with Doppler ultrasound, by measuring the conduit arterial diameter and the mean blood velocity averaged over consecutive cardiac beat-by-beat cycles (BB(cycle)) or muscle contraction-relaxation cycles (CR(cycle)). The precise impact fluctuations in the 1-BB(cycle)- or 1-CR(cycle)-rate may impose on the average blood flow measurements has previously not been clearly defined. The hypothesis investigated in the present study was that the blood flow measurements obtained, and its variability, during exercise, may differ between the 1-BB(cycle) and 1-CR(cycle) at incremental exercise intensities; as the BB(cycle)-measurements may be influenced by transient alterations in heart rate; whereas the CR(cycle)-measurements are dependent on the muscle contraction-relaxation frequencies independent of the exercise intensities per se. The main purpose was therefore to determine if fluctuations in blood flow for 1-BB(cycle) and 1-CR(cycle)varies at incremental exercise intensities (work rates) using the one-legged dynamic knee-extensor exercise (DKE) model. METHODS: Limb femoral artery blood flow (LBF) was determined, for 1-BB(cycle) and 1-CR(cycle), in 8 healthy male subjects during 4-min of steady-state DKE at 60 contractions per minute at 10, 20, 30 and 40 W. The variability of LBF was determined from the coefficients of variation (CVLBF). RESULTS: The CV(LBF) for the CR(cycle)-measurements at each work rate were similar (P=NS). The CV(LBF) for the BB(cycle)-measurements were higher (P<0.05) at 40 W compared to at 10 W. Furthermore, the CV(LBF) for the 1-BB(cycle) was higher (P<0.05) than for the 1-CR(cycle) at 30 and 40 W, despite almost identical mean LBF values for the BB(cycle)- and the CR(cycle)-measurements at each exercise intensity. CONCLUSIONS: The present data suggests that estimates of LBF at slightly higher exercise intensities such as above 30 W, for a few number of consecutive BB(cycle), renders a higher variability than for CR(cycle)-measurements. This may consequently result in slight over- and under-estimations of LBF compared to the CR(cycle)-measurement.

Adult↗
PubMed2004

Mechanisms mediating cholinergic antral circular smooth muscle contraction in rats.

AIM: To investigate the pathway (s) mediating rat antral circular smooth muscle contractile responses to the cholinomimetic agent, bethanechol and the subtypes of muscarinic receptors mediating the cholinergic contraction. METHODS: Circular smooth muscle strips from the antrum of Sprague-Dawley rats were mounted in muscle baths in Krebs buffer. Isometric tension was recorded. Cumulative concentration-response curves were obtained for (+)-cis-dioxolane (cD), a nonspecific muscarinic agonist, at 10(-8)-10(-4) mol/L, in the presence of tetrodotoxin (TTX, 10(-7) mol/L). Results were normalized to cross sectional area. A repeat concentration-response curve was obtained after incubation of the muscle for 90 min with antagonists for M1 (pirenzepine), M2 (methoctramine) and M3 (darifenacin) muscarinic receptor subtypes. The sensitivity to PTX was tested by the ip injection of 100 mg/kg of PTX 5 d before the experiment. The antral circular smooth muscles were removed from PTX-treated and non-treated rats as strips and dispersed smooth muscle cells to identify whether PTX-linked pathway mediated the contractility to bethanechol. RESULTS: A dose-dependent contractile response observed with bethanechol, was not affected by TTX. The pretreatment of rats with pertussis toxin decreased the contraction induced by bethanechol. Lack of calcium as well as the presence of the L-type calcium channel blocker, nifedipine, also inhibited the cholinergic contraction, with a reduction in response from 2.5+/-0.4 g/mm2 to 1.2+/-0.4 g/mm(2) (P<0.05). The dose-response curves were shifted to the right by muscarinic antagonists in the following order of affinity: darifenacin (M(3))>methocramine (M(2)) >pirenzepine (M(1)). CONCLUSION: The muscarinic receptors-dependent contraction of rat antral circular smooth muscles was linked to the signal transduction pathway(s) involving pertussis-toxin sensitive GTP-binding proteins and to extracellular calcium via L-type voltage gated calcium channels. The presence of the residual contractile response after the treatment with nifedipine, suggests that an additional pathway could mediate the cholinergic contraction. The involvement of more than one muscarinic receptor (functionally predominant type 3 over type 2) also suggests more than one pathway mediating the cholinergic contraction in rat antrum.

Anesthetics, Local↗