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PubMed1983

Psychophysiological response patterns in vascular and muscle-contraction headaches.

The psychophysiological response patterns of 43 headache subjects were compared to the response patterns of 11 nonheadache control subjects. The headache group was composed of subjects diagnosed as suffering from either muscle-contraction (N = 11), classic migraine (N = 11), common migraine (N = 11), or mixed (N = 10) headache. Discriminant analyses indicated that (1) the headache groups could be perfectly differentiated from the nonheadache control group after a period of relaxation and during a period of psychological stress and (2) the stress condition differentiated among the various headache groups. In general, the headache groups showed a higher level of arousal and were more responsive to stress. Also, the response pattern profiles differed among the headache groups in the stress condition. Muscle-contraction subjects tended to respond with higher frontal EMG, and classic migraine and mixed headache groups tended to respond with larger cardiovascular responses.

Adult↗

PubMed1991

Regulation of smooth muscle contraction in rabbit internal anal sphincter by protein kinase C and Ins(1,4,5)P3.

We have examined the role of protein kinase C (PKC)-beta II and its functional relationship to inositol 1,4,5-trisphosphate [Ins(1,4,5)P3] and intracellular Ca2+ in the contraction of smooth muscle cells from the rabbit internal and sphincter (IAS). PKC-beta (0.1-100 U/ml) and Ins(1,4,5)P3 (10(-9) to 10(-6) M) caused concentration-dependent contraction of IAS smooth muscle cells permeabilized by saponin. The combination of threshold concentrations of Ins(1,4,5)P3 (10(-9) M) and PKC (0.1 U/ml) was more than additive, causing near maximal shortening (28.2 +/- 2.1% decrease in cell length from control). The response to high concentrations of Ins(1,4,5)P3 and PKC used in combination was not greater than the response to either agent alone. The calmodulin antagonist W-7 (10(-9) M) inhibited the maximal contraction induced by Ins(1,4,5)P3 but not contraction caused by PKC, whereas the PKC antagonist H-7 (10(-6) M) inhibited the maximal contraction induced by PKC but not contraction caused by Ins(1,4,5)P3. Threshold doses of the ionophores A23187 (10(-9) M) and ionomycin (0.2 ng/ml) caused little contraction by themselves, but they potentiated the response elicited by a threshold concentration of PKC (0.1 U/ml), inducing maximal contraction. Preincubation of IAS cells with 4 mM Sr2+, which inhibits the release of intracellular Ca2+, abolished the potentiating effect of Ins(1,4,5)P3 and calcium ionophores on PKC, but the calmodulin antagonist W-7 did not. These data suggest that the contractile effect of maximally effective doses of PKC is independent of the effects of Ins(1,4,5)P3. At submaximal concentrations, however, PKC-dependent contraction is potentiated by Ins(1,4,5)P3 or by ionophore-mediated release of intracellular Ca2+ without requiring calmodulin activation.

Anal Canal↗

PubMed2005

Comparing condylar positions achieved through bimanual manipulation to condylar positions achieved through masticatory muscle contraction against an anterior deprogrammer: a pilot study.

STATEMENT OF PROBLEM: The condylar position can vary depending on several factors. One factor is the influence of occluding teeth. If the influence from occluding teeth could be eliminated, it might be possible to evaluate the condylar position obtained from masticatory muscle contraction. PURPOSE: The purpose of this pilot study was to determine the placement of the condyles by contracted masticatory muscles without influence from occluding teeth. MATERIAL AND METHODS: For a group of 11 participants, 3 dentists were assigned, in turn, to fabricate a centric relation interocclusal record using bimanual manipulation on each member of the group. After obtaining the centric relation interocclusal records using bimanual manipulation, the records were stored in room temperature water. Subsequently, each of the 11 patients had an anterior deprogrammer fabricated and were given instructions to wear the anterior deprogrammer for 60 minutes. The anterior deprogrammer was designed with the contacting surface perpendicular to the arc of close of the mandibular incisors. In addition, the anterior deprogrammer was relined to eliminate any movement under force, and the occluding surface of the deprogrammer was free of any indentations. After wearing the deprogrammer, 4 interocclusal records (3 in a reclined position and 1 in an upright position to ensure the condylar position did not change in the upright position) were made by having the patient squeeze and close into a properly adapted, trimmed, and warmed interocclusal record. The condylar position in centric relation recorded in interocclusal records using bimanual manipulation was compared to the condylar position recorded by the contraction of the masticatory muscles against an anterior deprogrammer using a condylar position indicating device. The data were analyzed with a 2-independent-samples test of proportions, alpha=.05 (1-tail). RESULTS: The condylar positions obtained using bimanual manipulation repeated the condylar position within the 0.11-mm tolerance of the Centri-Check instrument in 33 out of 33 opportunities (100%). The condylar positions obtained by using the anterior deprogrammer technique repeated the condylar position within the 0.11-mm tolerance of the Centri-Check in 43/44 opportunities (97.7%). The sample size used in this pilot study was not large enough to detect a very small actual difference (5 percentage points or less) between the 2 methods, should such a difference exist. CONCLUSION: The results of this pilot study indicate that, without influence from occluding teeth, the contraction of the masticatory muscles places the condyles into the same position as centric relation.

Centric Relation↗

PubMed2000

[Cellular mechanisms of smooth muscle contraction].

Myosin is an ATPase, able to form filaments with actin, thus initiating smooth muscle contraction (conversion of chemical energy into mechanical energy). Myosin activity is regulated by cytosolic calcium, via a calcium-calmodulin-MLCK-dependent phosphorylation. Extrusion of cytosolic calcium via calcium pumps (in the plasma membrane and sarcoplasmic reticulum) and via a sodium-calcium exchange allow smooth muscle cells to maintain their resting state. Constrictor agonists (hormones, neurotransmitters or drugs) act at membrane receptors inducing: (i) a fast and transient calcium mobilization from the sarcoplasmic reticulum, via phospholipase C (PLC) stimulation and inositol triphosphate (IP3) production or via a "calcium-induced calcium release" mechanism and opening of calcium channels in the sarcoplasmic reticulum and (ii) a slow and maintained mobilization of extracellular calcium, via the opening of voltage-dependent calcium channels in plasma membranes. Smooth muscle relaxation is ensured by a phosphatase which hydrolyzes phosphorylated myosin and decreases the calcium sensitivity of the contractile apparatus. Calcium signal is regulated at that level by: (i) protein kinase C, tyrosine kinase and arachidonic acid which inhibit phosphatase activity and (ii) cyclic AMP (cAMP) and cyclic GMP (cGMP) which enhance phosphatase activity. A second regulatory site is situated at the level of the non-contractile calcium compartment, which buffers signal transduction and where cGMP and/or cAMP enhance calcium extrusion mechanisms.

Calcium Signaling↗

PubMed1991

Airway blood flow modifies allergic airway smooth muscle contraction.

We tested the hypothesis that airway perfusion modifies the contractile response of airway smooth muscle to allergen challenge by influencing the clearance of locally released spasmogens. In six intact, lightly sedated, sheep allergic to Ascaris suum, we measured tracheal mucosal blood flow (Qtr) with a soluble gas uptake method and tracheal dead space (Vtr), an index of airway smooth muscle tone, by helium dilution before and serially after local aerosol challenge with A. suum extract or ragweed extract (control). The former challenge was repeated during continuous intravenous infusion of either vasopressin or nitroglycerin, which by themselves had no effect on Vtr and decreased and increased Qtr, respectively. Ragweed had no effect on Qtr and Vtr, whereas A. suum increased mean (+/- SE) Qtr by 111 +/- 31% (p less than 0.05) and decreased mean Vtr by 15 +/- 2% (p less than 0.05) immediately after challenge, with Qtr returning to baseline by 40 min and Vtr by 80 min. Vasopressin infusion prevented the A. suum-induced increase in Qtr and prolonged the decrease in mean Vtr (p less than 0.05). During nitroglycerin infusion, A. suum failed to alter Qtr or Vtr. Vasopressin and nitroglycerin had no effect on the contractile responses of tracheal smooth muscle to A. suum in vitro. These results indicate that the effects of vasopressin and nitroglycerin on antigen-induced airway smooth muscle contraction in vivo were due to alterations in airway blood flow rather than to alterations in the release of or airway smooth muscle responsiveness to chemical mediators.

Acetylcholine↗

PubMed1973

The mechanics of esophageal muscle contraction. Evidence of an inotropic effect of gastrin.

To compare the mechanical properties of lower esophageal sphincter (LES) and esophageal circular smooth muscle, force-velocity determinations were made under various physiological conditions. Isotonic and isometric recordings of opossum circular muscle were used to obtain the velocity of shortening and force, respectively, during alterations in: (a) initial muscle length (preload), (b) afterload, (c) calcium concentration, and (d) gastrin I. Muscle contraction was elicited to the neurogenic response at the termination of electrical stimulation. A change in preload (muscle length) altered the peak force (Po) developed during an afterloaded contraction, but had only a minor effect on the maximum velocity of shortening (V max). At the length of optimal tension development, Lo, (preload, 1.5 g), the LES muscle had a V max of 6.1+/-0.2 mm/s and a Po of 17.7+/-0.7 g. The esophageal muscle at its Lo (preload, 2.0 g) had a V max of 6.3+/-0.5 mm/s and a Po of 18.1+/-1.2 g. A decrease in calcium from 2.5 mM to 1.0 mM significantly reduced the V max and Po of all muscle, but an increase in calcium to 5.0 mM increased these parameters only minimally. At a calcium of 1.0 mM, gastrin I increased both V max and Po of all muscle. This inotropic effect of gastrin I occurred at lower concentrations in LES muscle than in muscle from the upper esophagus. The power (force x velocity) and work (force x muscle shortening) of esophageal and LES muscle were calculated from these data. Both the work and power generated during esophageal and LES muscle contraction were determined by: (a) the initial muscle length as produced by the preload, (b) the afterload against which the muscle was contracting, and (c) the contractility of inotropism of the muscle, that is, the force-velocity curve on which the muscle was operating.

Animals↗

PubMed2006

Muscle-contraction properties in overarm throwing movements.

On the basis of dynamic and kinematic data, this study identifies the type of muscle contraction in unloaded overarm throwing movements. An unloaded throw or nearly unloaded throw is defined as the throw in which the external resistance is too small (e.g., the team handball, baseball, and water polo throws as well as the tennis and badminton smashes). A special arm-force-measuring apparatus was constructed to imitate an overarm throw. Forty-two subjects were placed into 3 groups: untrained subjects, weight-trained athletes, and team handball players. The measured parameters included the velocity of the initial movement, the release velocity, the velocity of the first 50 milliseconds of the concentric phase, the force value at the moment of deceleration of the initial movement, and the impulse values during the eccentric and concentric phases of the test movement. Statistically significant higher values of the above parameters (p < 0.05) were determined in that test at which the initial speed of movement was higher. Also, the correlation coefficients of the parameters of the initial phase of the throw movement were very high (p < 0.001), especially the parameters related with the movement's first 50 milliseconds. The results support the thesis that the stretch-shortening cycle is the type of muscle contraction in unloaded overarm throws. Furthermore, it is possible to increase the throw velocity by increasing the velocity of the initial movement (i.e., by provoking higher inertia forces).

Acceleration↗

PubMed1992

[The effect of ionized calcium concentration on muscle contraction and on the effect of non-depolarizing neuromuscular blocking agent].

The influence of serum ionized calcium (Ca2+) on the muscle contraction and on the effect of non-depolarizing neuromuscular blocking agent, d-tubocurarine (dTc), was investigated. The isolated phrenic nerve-diaphragma preparation of the rat was stimulated directly and indirectly at 0, 0.4, 0.7, 1.4, 2.5 mM of total calcium concentration (Ca2+: 0, 0.39, 0.52, 1.12, 2.32 mM, respectively). With indirect stimulation, no contraction was observed from 0 to 0.4 mM of calcium, but the twitch tension returned to 100 percent of control at over 0.7 mM of calcium. However, with direct stimulation, the twitch tension was obtained up to 100 percent of control independent of Ca2+ concentration. The ED50 of dTc was correlated well with the serum Ca2+. These findings suggest that the decrease of serum Ca2+ concentration interferes with the muscle contraction and potentiates the effect of dTc. We speculate that the site of its action may be primarily prejunctional.

Animals↗

PubMed1992

Actin mediated regulation of muscle contraction.

Striated and smooth muscles have different mechanisms of regulation of contraction which can be the basis for selective pharmacological alteration of the contractility of these muscle types. The progression in our understanding of the tropomyosin-troponin regulatory system of striated muscle from the early 1970s through the early 1990s is described along with key concepts required for understanding this complex system. This review also examines the recent history of the putative contractile regulatory proteins of smooth muscle, caldesmon and calponin. A contrast is made between the actin linked regulatory systems of striated and smooth muscle.

Actins↗

PubMed2006

[Capacitative Ca²⁺ entry is involved in ACh-induced distal colon smooth muscle contraction in rats].

Contraction of smooth muscle cells is triggered by an increase in cytosolic Ca(2+) upon agonist stimulation. Ca(2+) influx across the plasma membrane constitutes a major component of the agonist-induced response in smooth muscle cells. Traditionally, voltage-operated Ca(2+) channel (VOCC) is considered as the channel mediating the Ca(2+) entry. However, this view has been challenged by recent discoveries, which demonstrated that other types of ion channels, such as store-operated and/or receptor-operated Ca(2+) channels (SOCC and/or ROCC), also participate in Ca(2+) response induced by agonists in smooth muscle cells. SOCC is defined as the channel activated in response to the depletion of the internal Ca(2+) stores, an event secondary to G protein coupled receptor or receptor tyrosine kinase stimulation. The Ca(2+) flow mediated by SOCC is termed as capacitative Ca(2+) entry (CCE). Previous study from other group has demonstrated that VOCC played a predominant role in ACh-induced contraction of distal colon smooth muscle in guinea pig. However, whether SOCC participates in the agonist-induced contractile response in this particular tissue is unknown. The present study was performed to investigate the role of CCE in ACh-induced mechanical activity of distal colon smooth muscle in rats. The contractile function of the smooth muscle was assessed by measuring isometric force of isolated rat distal colon rings. We showed that both high extracellular K(+) (40 mmol/L) and ACh (5 mumol/L) evoked striking contraction of the smooth muscle. The contractile responses were almost abolished by removal of extracellular Ca(2+) with ethylene glycol-bis(2-aminoethylether)-N,N,N',N' tetraacetic acid (EGTA), suggesting a critical contribution of extracellular source of Ca(2+) to the contraction. Verapamil (5 mumol/L), an L-type VOCC blocker, significantly attenuated, but didn't completely eliminate the high K(+)- and ACh-induced contraction (74% and 41% for high K(+) and ACh, respectively), indicating that additional channels might be involved in the contractile mechanism. Furthermore, ACh only induced transient contractions in the absence of extracellular Ca(2+). Readmission of Ca(2+) into the extracellular compartment resulted in a significant and sustained increase in the tension of the smooth muscle. This response was not affected by verapamil (5 mumol/L) and Cd(2+) (5 mumol/L), both of which efficiently block VOCC at the doses. However, La(3+), a known inhibitor of SOCC, significantly suppressed the Ca(2+) readdition-induced contraction in a dose-dependent manner. On the basis of these results, we conclude that contraction of smooth muscle in the distal colon is regulated by multiple Ca(2+) channels. In addition to VOCC-mediated Ca(2+) influx, SOCC-mediated CCE participates in agonist-induced contractile response of distal colon smooth muscle in rats.

Acetylcholine↗

PubMed2001

Insulin increases FA uptake and esterification but reduces lipid utilization in isolated contracting muscle.

We examined the effect of insulin on the synthesis and degradation of muscle lipid pools [phospholipid (PL), diacylglycerol (DG), triacylglycerol (TG)] and palmitate oxidation in isolated resting and contracting (20 tetani/min) soleus muscles. Lipid metabolism was monitored using the previously defined pulse-chase procedure. At rest, insulin significantly increased total palmitate uptake into soleus muscle (+49%, P < 0.05), corresponding to enhanced DG (+60%, P < 0.05) and TG (+61%, P < 0.05) esterification, but blunted palmitate oxidation (-38%, P < 0.05) and TG hydrolysis (-34%, P < 0.05). During muscle contraction, when total palmitate uptake was increased, insulin further enhanced uptake (+21%, P < 0.05) and esterification of fatty acids (FA) to PL (+73%, P < 0.05), DG (+19%, P < 0.05), and TG (+161%, P < 0.01). Despite a profound shift in the relative partitioning of FA away from esterification and toward oxidation during contraction, the increase in palmitate oxidation and TG hydrolysis was significantly blunted by insulin [oxidation, -24% (P = 0.05); hydrolysis, -83% (P < 0.01)]. The effects of insulin on FA esterification (stimulation) and oxidation (inhibition) during contraction were reduced in the presence of the phosphatidylinositol 3-kinase inhibitor LY-294002. In summary, the effects of insulin and contraction on palmitate uptake and esterification are additive, while insulin opposes the stimulatory effect of contraction on FA oxidation and TG hydrolysis. Insulin's modulatory effects on muscle FA metabolism during contraction are mediated at least in part through phosphatidylinositol 3-kinase.

Animals↗

PubMed1983

Smooth muscle contracting compounds in venoms of sphecid wasps (Hym: Sphecidae).

1. The presence of smooth muscle contracting substances in venom preparations made from six species of sphecid wasps was investigated using a number of standard pharmacological techniques. 2. In addition, acetylcholine was identified by enzymatic degradation as well as by mass fragmentography, while histamine was determined using a radio-enzymatic method. 3. The venom reservoir of P. triangulum contains about 400 ng acetylcholine, but no histamine-, 5-HT- or bradykinin-like activity. 4. The venoms of the five other species contain histamine in amounts varying from 20 to 2000 ng per venom reservoir, but no acetylcholine-, 5-HT- or bradykinin-like activity.

Acetylcholine↗

PubMed2005

Rapid inhibitory effect of glucocorticoids on airway smooth muscle contractions in guinea pigs.

The common disease asthma is characterized by the obstruction, inflammation and increased sensitivity of the airways. Glucocorticoids (GCs) are one of the most potent anti-inflammatory agents available for treating allergic disease. In this study, we report that the GC budesonide (BUD) can rapidly inhibit the histamine-induced contractions of airway smooth muscle in a process mediated by non-genomic mechanisms. The tracheas of albino Hartley guinea pigs were used. We measured the effects of BUD on the increased isometric tension of trachea segment rings and the shrinking of single airway smooth muscle cells (ASMCs) induced by histamine. With the application of each reagent, the changes in the isometric tension of the segment rings upon maximum contraction and at four time points were recorded. We found that BUD significantly suppressed the increase in isometric tension induced by histamine in guinea pigs within 15 min. We also observed that BUD can reduce the histamine-induced shrinking of single ASMCs in an even shorter time. Mifepristone (RU486) and actidione did not depress the inhibitory effect of BUD. The results preclude action via genomic-mediated responses that usually take several hours to occur. We conclude therefore that GCs have a rapid non-genomic inhibitory effect on guinea pig airway smooth muscle contractions, and provide a new way to investigate this non-genomic mechanism. Further study can provide theoretical evidence for the clinical application of GCs in asthma and other allergic diseases.

Animals↗

PubMed1975

Some self-consistent two-state sliding filament models of muscle contraction.

The general formalism required to treat two-state sliding filament models of muscle contraction, including free energy considerations, is first reviewed and amplified. This formalism is then used to examine, and modify as needed, three models studied previously by Podolsky and Nolan, in which cross-bridge attachment-detachment and ATP turnover are not tightly coupled. No attempt is made here to establish an optimal, self-consistent model of this type because our interest is primarily in methadology rather than in fitting experimental results. But it appears from this preliminary study that such a model, with satisfactory mechanical and thermodynamic properties, could be found. An extremely simple but unrealistic two-state model is also studied which is of interest because it demonstrates the fact that it is possible, in principle at least, for sliding filament models to work with very high thermodynamic efficiencies (50-100 percent). An appendix is included that is concerned with the form of the dependence of certain first-order rate constants on the concentrations of ATP, ADP, and P.

Adenosine Diphosphate↗

PubMed1994

Lactate transport in rat sarcolemmal vesicles and intact skeletal muscle, and after muscle contraction.

To determine whether it was possible to measure lactate transport rates into intact skeletal muscles, the transport of lactate (zero-trans) was determined in soleus muscle strips incubated in vitro and compared with lactate transport in sarcolemmal vesicles. In addition, the effects of muscle contractility on lactate transport were investigated in electrically-stimulated soleus muscle strips. In both the intact muscle and the sarcolemmal preparations the rates of transport were saturable, stereospecific, and inhibitable by monocarboxylates (pyruvate, alpha-cyano-4-hydroxycinnamate) and a protein modifier (N-ethylmaleimide; P < 0.05). The anion exchange inhibitor SITS had no effect on lactate uptake (P > 0.05). In both preparations lactate transport followed an inwardly directed proton gradient. Relative comparisons (%) between the preparations indicated a similar slope of increasing transport rates with increasing lactate concentrations and similar responses to a changing pH environment. These characterizations of L-lactate transport into isolated sarcolemmal vesicles and muscle strips revealed that both preparations yielded similar conclusions regarding the transmembrane movement of L-lactate. By using this more physiological muscle preparation, contractile activity, induced by electrical stimulation, did not increase lactate uptake in skeletal muscle in the post-exercise period whereas under similar conditions a marked increase in 2-deoxy-D-glucose uptake occurred (+ 47%; P < 0.05). These data suggest that the transport of glucose and lactate in contracting muscle is regulated differently. These studies also show that the incubated muscle strip preparation may be useful for studying lactate transport in an intact cell system during physiological experiments.

Animals↗

PubMed1997

Temporal effect of muscle contraction on respiratory sinus arrhythmia.

The purpose of this investigation was to compare the heart rate variability at respiratory frequency (HRVRF) in muscle contractions during the inspiratory phase with that during the expiratory phase. Eight volunteers performed pedaling on a cycle ergometer, twice a cycle of respiration (4 sec) against a load of 0.25 Nm/kg BW, of which the timing was adjusted to twice during the inspiration phase (I), once during the expiration, once during the inspiration (EI), or twice during the expiration phase (E). Spectral analysis was applied to the R-R intervals of each condition. The amplitude of HRVRF in E was less than half of 1 (9 +/- 2 msec versus 23 +/- 2 msec). The results indicate that the timing of muscle contraction can affect the heart rate variability even at the frequency band of respiration.

Adult↗

PubMed1993

Biochemical characterization of a vascular smooth muscle contracting polypeptide purified from Phoneutria nigriventer (armed spider) venom.

Biochemical characterization of a vascular smooth muscle contracting polypeptide purified from Phoneutria nigriventer (armed spider) venom. Toxicon 31, 377-384, 1993. Crude Phoneutria nigriventer venom was fractionated by Sephadex, ion-exchange and reverse-phase high performance liquid chromatography. One protein (PNV1) with spasmogenic activity in rabbit vascular smooth muscle was isolated and biochemically characterized. PNV1 has 125 amino acid residues and a calculated mol. wt of 13,899. Special features of the amino acid composition of PNV1 are the presence of two disulfide bridges and the high percentage (27%) of Asx and Glx. The N-terminal amino acid sequence indicates that PNV1 is different from other polypeptides isolated from Phoneutria nigriventer venom.

Amino Acid Sequence↗

PubMed2001

Extracellular formation and uptake of adenosine during skeletal muscle contraction in the rat: role of adenosine transporters.

1. The existence of adenosine transporters in plasma membrane giant vesicles from rat skeletal muscles and in primary skeletal muscle cell cultures was investigated. In addition, the contribution of intracellularly or extracellularly formed adenosine to the overall extracellular adenosine concentration during muscle contraction was determined in primary skeletal muscle cell cultures. 2. In plasma membrane giant vesicles, the carrier-mediated adenosine transport demonstrated saturation kinetics with Km = 177 +/- 36 microM and Vmax = 1.9 +/- 0.2 nmol x ml(-1) x s(-1) (0.7 nmol (mg protein)(-1) x s(-1)). The existence of an adenosine transporter was further evidenced by the inhibition of the carrier-mediated adenosine transport in the presence of NBMPR (nitrobenzylthioinosine; 72% inhibition) or dipyridamol (64% inhibition; P < 0.05). 3. In primary skeletal muscle cells, the rate of extracellular adenosine accumulation was 5-fold greater (P < 0.05) with electrical stimulation than without electrical stimulation. Addition of the adenosine transporter inhibitor NBMPR led to a 57% larger (P < 0.05) rate of extracellular adenosine accumulation in the electro-stimulated muscle cells compared with control cells, demonstrating that adenosine is taken up by the skeletal muscle cells during contractions. 4. Inhibition of ecto-5'-nucleotidase with AOPCP in electro-stimulated cells resulted in a 70% lower (P < 0.05) rate of extracellular adenosine accumulation compared with control cells, indicating that adenosine to a large extent is formed in the extracellular space during contraction. 5. The present study provides evidence for the existence of an NBMPR-sensitive adenosine transporter in rat skeletal muscle. Our data furthermore demonstrate that the increase in extracellular adenosine observed during electro-stimulation of skeletal muscle is due to production of adenosine in the extracellular space of skeletal muscle and that adenosine is taken up rather than released by the skeletal muscle cells during contraction.

Adenosine↗