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PubMedDate not supplied

Effects of Elevated Cytosolic Calcium on ACh-Induced Swine Tracheal Smooth Muscle Contraction.

Increased intracellular calcium concentration ([Ca(2+)](i)) is required for smooth muscle contraction. In tracheal and other tonic smooth muscles, contraction and elevated [Ca(2+)](i) are maintained as long as an agonist is present. To evaluate the physiological role of steady-state increases in Ca(2+) on tension maintenance, [Ca(2+)](i) was elevated using ionomycin, a Ca(2+) ionophore or charybdotoxin, a large-conductance calcium-activated potassium channel (K(Ca)) blocker prior to or during exposure of tracheal smooth muscle strips to ACh (10(-9) to 10(-4) M). Ionomycin (5 &mgr;M) in resting muscles induced increases in [Ca(2+)](i) to 500 +/- 230 nM and small increases in force of 2.6 +/- 2.3 N/cm(2). This tension is only 10% of the maximal tension induced by ACh. Charybdotoxin had no effect on [Ca(2+)](i) or tension in resting muscle. After pretreatment of muscle with ionomycin, the concentration-response relationship for ACh-induced changes in tension shifted to the left (EC(50) = 0.07 +/- 0.05 &mgr;M ionomycin; 0.17 +/- 0.07 &mgr;M, control, p < 0.05). When applied to the muscles during steady-state responses to submaximal concentrations of ACh, both ionomycin and charybdotoxin induced further increases in tension. The same magnitude increase in tension occurs after ionomycin and charybdotoxin treatment, even though the increase in [Ca(2+)](i) induced by charybdotoxin is much smaller than that induced by ionomycin. We conclude that the resting muscle is much less sensitive to elevation of [Ca(2+)](i) when compared to muscles stimulated with ACh. Steady-state [Ca(2+)](i) limits tension development induced by submaximal concentrations of ACh. The activity of K(Ca) moderates the response of the muscle to ACh at concentrations less than 1 &mgr;M. Copyright 1996 S. Karger AG, Basel

Journal Article↗

PubMed2003

The effect of muscle contraction velocity on cardiorespiratory responses to repetitive isokinetic exercise in humans.

We investigated the effect of muscle contraction velocity on cardiorespiratory responses during exercise. Eight males (23 +/- 2 years, 175 +/- 5 cm, 64 +/- 6 kg, mean +/- SD) performed 3-min repetitive one-leg extension exercises at various angular velocities (30, 60, 120, and 240 deg/s) with a controlled relaxation interval, relatively constant (duty cycle = 1:1, A trial) and absolutely constant (relaxation time = 0.75 s, B trial) at a total work of 2,100-2,400 J in an isokinetic mode, using a Cybex II dynamometer. We measured heart rate (HR), mean blood pressure (MAP), minute ventilation (Vdot;E), and oxygen uptake (Vdot;O(2)) during the exercise. The angular velocity significantly affected the increase in HR, MAP, Vdot;E, and Vdot;O(2) at the end of exercise from resting in both A and B trials (e.g., MAP: 12 +/- 2, 10 +/- 2, 11 +/- 2, and 18 +/- 2 mmHg in the A trial). The result suggests that muscle contraction velocity affects cardiorespiratory responses during repetitive isokinetic exercise.

Adult↗

PubMed1997

Interleukin-1beta-induced, nitric oxide-dependent and -independent inhibition of vascular smooth muscle contraction.

Stimulation of vascular smooth muscle by bacterial lipopolysaccharide has been shown to produce interleukin-1beta and to induce vasodilation in septic shock. To understand the mechanisms of interleukin-1beta-induced relaxation, we examined the effects of interleukin-1beta on contractility and cyclic GMP contents of vascular smooth muscle. After treatment of the rat aorta with interleukin-1beta (20 ng/ml) for 6 h, the cyclic GMP content increased and the contraction induced by phenylephrine (1 microM) was partially inhibited. An inhibitor of nitric oxide (NO) synthase, N(G)-monomethyl-L-arginine (L-NMMA, 100 microM), prevented the inhibitory effect of interleukin-1beta. After treatment with interleukin-1beta for 24 h, the phenylephrine-induced contraction was inhibited more strongly. Neither L-NMMA (100 microM) nor aminoguanidine (100 microM) reversed the inhibition, whereas methylene blue (10 microM) partially reversed the inhibition. After treatment with interleukin-1beta for 12 or 24 h, the cyclic GMP content increased but to a level lower than that obtained with a 6-h treatment. The effects of sodium nitroprusside (1 microM) to inhibit the phenylephrine-induced contraction and to increase the cyclic GMP content were markedly suppressed by the 24-h interleukin-1beta treatment. In contrast, the 24-h interleukin-1beta treatment did not change the ability of 8-bromo-cGMP to relax the phenylephrine-stimulated aorta. Addition of L-NMMA (1 mM) during the 24 h treatment prevented NO production and preserved the sodium nitroprusside-induced cGMP generation by interleukin-1beta. The 24 h interleukin-1beta treatment increased the threshold concentration of KCl needed to induce contraction without changing the maximum contraction. In the presence of 25.4 mM KCl or the non-selective K+ channel inhibitor, tetraethylammonium, the inhibitory effect of the 24-h interleukin-1beta treatment on phenylephrine-induced contraction was restored. These results suggest that interleukin-1beta inhibits vascular smooth muscle contraction by a time-dependent, dual mechanism. After a 6-h treatment with interleukin-1beta, the NO/cyclic GMP system is activated. After a 24-h interleukin-1beta treatment, in contrast, the NO/cyclic GMP system may be desensitized and the contraction of vascular smooth muscle is inhibited by another mechanism, possibly membrane hyperpolarization.

Animals↗

PubMed2005

Reflex muscle contraction in the unaware occupant in whiplash injury.

STUDY DESIGN: Computer modeling and parametric analysis were used to determine the effect of reflex contraction of the neck muscles in the unaware occupant in whiplash. OBJECTIVE: To delineate effects of reflex contraction on spinal segmental kinematics during the retraction phase. SUMMARY OF BACKGROUND DATA: The ability of reflex neck muscle contraction to mitigate whiplash injury in the unaware occupant remains unclear. Analyzing relative timing between electromyographic and head-neck kinematics, previous investigators theorized that muscle contraction alters spinal kinematics, decreasing injury likelihood. Other investigators suggested that injury occurs during the initial (retraction) phase of head-neck kinematics, before significant muscle force generation. METHODS: Computer modeling was used to determine reflex contraction effects on segmental angulations, implementing parametric analysis techniques to vary reflex delay and impact severity. RESULTS: Shorter reflex delays had a greater effect on segmental angulations later in the event and at lower impact severities. However, the magnitude of this effect, particularly at higher impact severities and during maximum cervical S-curvature (factors implicated in the whiplash injury mechanism) was minimal, altering segmental angulations by a maximum of 19%. CONCLUSIONS: Because reflex contraction did not substantially alter spinal kinematics, muscle contraction likely does not initiate in sufficient time to mitigate whiplash injuries that may occur during the retraction phase.

Cervical Vertebrae↗

PubMed1986

The role of tropomyosin-troponin in the regulation of skeletal muscle contraction.

Steric blocking of actin-myosin interaction by tropomyosin has been a working hypothesis in the study of the regulation of skeletal muscle contraction, yet the simple movement of actin-associated tropomyosin from a myosin-blocking position (relaxation) to a nonblocking position (contraction) cannot adequately account for all of the biophysical and biochemical observations which have been made to date. Ambiguous assignment of tropomyosin positions on actin during contraction, due in part to the limited resolution of reconstruction techniques, may also hint at a real lack of clearcut 'on' and 'off' positioning of tropomyosin and tropomyosin-troponin complex. Recent biochemical evidence suggests processes relatively independent of tropomyosin-troponin may have a governing effect on contraction, involving kinetic constraints on actin-myosin interaction influenced by the binding of ATP and the intermediates of ATP hydrolysis. Based on our current understanding put forth in this review, it is clear that regulatory interactions in muscle contraction do not consist solely of steric effects but involve kinetic factors as well. Where the latter are being defined in systems reconstituted from purified proteins and their fragments, the steric components of regulation are most clearly observed in studies of structurally more intact physiologic systems (e.g. intact or skinned whole muscle fibres). The fine detail of the processes and their interplay remains an intriguing question. Likewise, the precise physical relationship of myosin with actin in the crossbridge cycle continues to elude definition. Refinement of several methodologies (X-ray crystallography, three-dimensional reconstruction, time-resolved X-ray diffraction) will increase the potential for detailing the molecular basis of the regulation of muscle contraction.

Actins↗

PubMed2000

Effects of muscle contraction on the load-strain properties of frog aponeurosis and tendon.

The mechanical properties of the frog semitendinosus (ST) tendon and aponeurosis were measured during passive tensile loading to a force equal to ST maximum tetanic tension and during active isometric muscle contraction. During active contraction, both the tendon and aponeurosis regions initially strained at rates exceeding 400%/s while near the end of the muscle contraction, strain rates were nearly zero. At this point, the strain in the tendon region was equal to that observed during slow passive loading to the same tension level. However, for the aponeurosis, even near the zero strain rate, strain at the end of the active contraction was significantly below that observed during slow passive loading (p < 0. 001). Specifically, when aponeurosis strain rate was almost zero, aponeurosis strain was 13.8 +/- 3% (means +/- SEM, n = 10), which was significantly below that measured during passive loading (23.7 +/- 5%) suggesting that active contraction actually altered aponeurosis material properties. These data demonstrate that, while the tendon and aponeurosis regions have different passive biomechanical properties and both demonstrate viscosity typical of other connective tissues, the aponeurosis region of the frog ST actually changed its intrinsic properties during muscle contraction. Thus, extrapolation of biomechanical data obtained at nonphysiological strain rates or under conditions where the muscle-tendon junction has been interrupted should be made with caution.

Animals↗

PubMed1991

[Inhibition of airway smooth muscle contraction by airway epithelium in human bronchus].

To clarify the mechanism underlying the inhibitory effect of epithelial cells on smooth muscle contraction, we studied two types of human bronchial tissue preparations: (1) "acceptor" bronchial strip without epithelium, (2) "donor" bronchial ring with or without epithelium. We measured the contractile responses of acceptor bronchial strip surrounded by donor bronchial ring to increasing concentrations of acetylcholine (ACh). Removal of the epithelium of the donor bronchial rings significantly enhanced the contractions of the acceptor bronchial strips. Thus, airway epithelium decreases the airway smooth muscle contraction to ACh in human bronchus. The mechanism of this inhibitory effect of airway epithelium was not due to a change in mechanical property of the airway, nor to a change in diffusion path for the chemical mediators. These results suggest that human airway epithelium may have an important role in modulating airway smooth muscle tone, possibly by the release of an epithelium-derived relaxing factor.

Acetylcholine↗

PubMed1992

Involvement of rho p21 in the GTP-enhanced calcium ion sensitivity of smooth muscle contraction.

In the rabbit mesenteric arterial smooth muscle skinned by saponin, Ca2+ induced contraction in a concentration-dependent manner. Guanosine 5'-(3-O-thio)triphosphate (GTP gamma S), a non-hydrolyzable GTP analogue, lowered the Ca2+ concentrations required for this contraction and increased the Ca2+ sensitivity of the skinned smooth muscle contraction. GTP gamma S alone did not induce the contraction in the absence of Ca2+. This GTP gamma S-enhanced Ca2+ sensitivity was completely abolished by an exoenzyme of Staphylococcus aureus, named EDIN, and an exoenzyme of Clostridium botulinum, named C3, both of which are known to ADP-ribosylate the rho p21 family that belongs to the ras p21-like small GTP-binding protein superfamily. The GTP gamma S-bound form of rhoA p21 overcame the inhibitory action of EDIN. smg p21B, another small GTP-binding protein, was inactive. EDIN ADP-ribosylated a protein, which was most likely to be rho p21, in the skinned smooth muscle. The GTP gamma S-bound form of rhoA p21, but not the GDP-bound form, substituted for GTP gamma S and enhanced the Ca2+ sensitivity of the skinned smooth muscle contraction. smg p21B was inactive. These results indicate that rhoA p21 is involved in the GTP gamma S-enhanced Ca2+ sensitivity of the smooth muscle contraction.

Adenosine Diphosphate Ribose↗

PubMed1995

Kinase activation and smooth muscle contraction in the presence and absence of calcium.

PURPOSE: The intracellular signalling mechanisms that modulate the sustained vascular smooth muscle contractions that occur with vasospasm are not well understood. The purpose of this investigation was to examine cell signalling mechanisms that account for sustained vascular smooth muscle contraction, independent of increases in intracellular Ca2+ concentrations ([Ca2+]i). METHODS: Fresh bovine carotid artery smooth muscles contractile responses were examined in a muscle bath. [Ca2+]i was depleted by use of the extracellular Ca2+ chelator, ethylene glycol-bis(beta-aminoethylether) N,N,N',N'-tetraacetic acid and the intracellular chelator, 1,2-bis(2-aminophenoxy)ethane-N,N,N',N',-tetraacetic acid. RESULTS: In Ca(2+)-free conditions, depolarizing the membrane with high extracellular KCI failed to elicit a contraction. In addition, in Ca(2+)-free conditions the ([Ca2+]i) was less than 10 nmol/L as determined with the Ca(2+)-indicator, Fura 2. The protein kinase C (PKC) activator, phorbol 12, 13-dibutyrate (PDBu), induced slowly developing sustained contractions in bovine carotid artery smooth muscle, and the magnitude of the contractile response to PDBu (10 nmol/L to 10 mumol/L) was the same in the presence and absence of Ca2+. PDBu induced contractions in Ca(2+)-free conditions were not inhibited by the myosin light chain kinase inhibitor, ML-9 (50 mumol/L), but were inhibited by the PKC inhibitor, staurosporine (50 nmol/L). CONCLUSIONS: These data suggest that vascular smooth muscle contractions can occur under conditions where the [Ca2+]i is low and fixed and that these contractions may be mediated by PKC.

15-Hydroxy-11 alpha,9 alpha-(epoxymethano)prosta-5↗

PubMedDate not supplied

Effects of sodium channel blockers on electrical field stimulation-induced guinea-pig tracheal smooth muscle contraction.

The effects of sodium channel blockers, a conventional one: tetrodotoxin, and clinically available ones: cibenzoline, flecainide and SUN 1165 [N-(2,6-dimethylphenyl)-8-pyrrolizidine-acetamide hydrochloride hemihydrate] on electrical field stimulation-induced and carbachol-induced guinea-pig tracheal smooth muscle contraction were investigated. Electrical field stimulation was performed at 50 V with 20 Hz and 0.8 msec square pulse duration. Carbachol (5 x 10(-8) M) was used for induction of tracheal contractions. All agents were administered before electrical field stimulation or carbachol administration. Electrical field stimulation-induced tracheal smooth muscle contraction was dose-dependently reduced by all sodium channel blockers used. The effects of sodium channel blockers on electrical field stimulation-induced contraction were greater than those on carbachol-induced contractions, except for SUN 1165 which reduced similarly both electrical field stimulation- and carbachol-induced contractions. These results indicate that the sodium influx is closely related to the acetylcholine release, resulting in smooth muscle contraction. Since the parasympathetic nervous system may be involved in the genesis of various pathological conditions, such as bronchial asthma, sodium channel blockers could contribute to the management of these conditions.

Animals↗

PubMed2001

Mitogen-activated protein kinase signal transduction in skeletal muscle: effects of exercise and muscle contraction.

Exercise has numerous growth and metabolic effects in skeletal muscle, including changes in glycogen metabolism, glucose and amino acid uptake, protein synthesis and gene transcription. However, the mechanism(s) by which exercise regulates intracellular signal transduction to the transcriptional machinery in the nucleus, thus modulating gene expression, is largely unknown. This review will provide insight on potential intracellular signalling mechanisms by which muscle contraction/exercise leads to changes in gene expression. Mitogen-activated protein kinase (MAPK) cascades are associated with increased transcriptional activity. The MAPK family members can be separated into distinct parallel pathways including the extracellular signal-regulated kinase (ERK) 1/2, the stress-activated protein kinase cascades (SAPK1/JNK and SAPK2/p38) and the extracellular signal-regulated kinase 5 (ERK5). Acute exercise elicits signal transduction via MAPK cascades in direct response to muscle contraction. Thus, MAPK pathways appear to be potential physiological mechanisms involved in the exercise-induced regulation of gene expression in skeletal muscle.

Animals↗

PubMed2000

Cortico-muscular synchronization during isometric muscle contraction in humans as revealed by magnetoencephalography.

Magnetoencephalographic (MEG) and electromyographic (EMG) signals were recorded from six subjects during isometric contraction of four different muscles. Cortical sources were located from the MEG signal which was averaged time-locked to the onset of motor unit potentials. A spatial filtering algorithm was used to estimate the source activity. Sources were found in the primary motor cortex (M1) contralateral to the contracted muscle. Significant coherence between rectified EMG and M1 activity was seen in the 20 Hz frequency range in all subjects. Interactions between the motor cortex and spinal motoneuron pool were investigated by separately studying the non-stationary phase and amplitude dynamics of M1 and EMG signals. Delays between M1 and EMG signals, computed from their phase difference, were found to be in agreement with conduction times from the primary motor cortex to the respective muscle. The time-dependent cortico-muscular phase synchronization was found to be correlated with the time course of both M1 and EMG signals. The findings demonstrate that the coupling between the primary motor cortex and motoneuron pool is at least partly due to phase synchronization of 20 Hz oscillations which varies over time. Furthermore, the consistent phase lag between M1 and EMG signals, compatible with conduction time between M1 and the respective muscle with the M1 activity preceding EMG activity, supports the conjecture that the motor cortex drives the motoneuron pool.

Adult↗

PubMed2005

Effects of effort and EMG levels on short-latency stretch reflex modulation after varying background muscle contractions.

It is known that the short-latency stretch reflex (SLSR) is modulated by the background muscle activity when it is elicited at matched torque levels. This study was designed to examine the effects of muscle contraction types before a stretch perturbation on SLSR in the human soleus muscle (SOL) when SLSR was elicited at the same levels of effort and at matched electromyographic (EMG) activity levels. A mechanical stretch perturbation was applied to the calf muscles when the ankle joint reached a ninety degree tibio-tarsal joint angle after the muscles performed an isometric (pre-ISO), shortening (pre-SHO) and lengthening contraction (pre-LEN). Subjects were seated on an ankle ergometer chair and developed 0%, 10%, 20%, 30%, 40%, 50%, 60% and 70% ankle joint torque (AJT) of maximum voluntary isometric plantar flexion contraction at 80 degrees in pre-SHO, at 90 degrees in pre-ISO and at 100 degrees in pre-LEN. After that, isometric or dynamic contractions started, and the subjects were asked to maintain effort levels as, needed, to maintain the target torque levels until the end of the stretch. They relaxed their muscles fully after the stretch. This chain of processes was consecutively repeated 10 times. EMG signals obtained from SOL were averaged after they were high-pass filtered and full-wave rectified. Some major findings resulted: (1) there were no differences in SLSR area in the active muscle between pre-ISO and pre-SHO, whereas its waveform was steeper in pre-ISO than in pre-SHO. (2) SLSR p-to-p amplitude and waveform were larger and steeper in the active muscle than in the relaxed one in all conditions, whereas they were independent of the effort levels once the muscle was activated. This led to steady SLSR modulation in response to the background muscle contraction in the active muscle regardless of whether the SLSR was elicited at matched AJT or EMG activity levels. These findings suggest that SLSR is closely related to the muscle spindle sensitivity influenced by the following factors: (1) the background muscle contraction type, and (2) gamma motoneuron activity set by CNS based on the effort level.

Adaptation, Physiological↗

PubMed2006

Ia-afferent input to motoneurons during shortening and lengthening muscle contractions in humans.

The central nervous system employs different strategies to execute specific motor tasks. Because afferent feedback during shortening and lengthening muscle contractions differs, the neural strategy underlying these tasks may be quite distinct. Cortical drive may be adjusted or afferent input regulated. The exact mechanisms are not clear. Here, we examine the control of synaptic transmission across the Ia synapse during shortening and lengthening muscle contractions. Subjects were instructed to maintain isolated activity in a single tibialis anterior (TA) motor unit while muscle length was varied from flexion to extension and back. At a fixed interval after a firing of the active motor unit, a single electrical stimulus was applied to the common peroneal nerve to activate Ia afferents from the TA muscle. We investigated the stimulus-induced change in firing probability of 19 individual low-threshold TA motor units during shortening and lengthening contractions. Any change in firing probability depends on both pre- and postsynaptic mechanisms. In this experiment, motoneuron firing rate was similar during both contraction types. There was no difference in the firing probability between shortening and lengthening contractions (0.23 +/- 0.03 and 0.20 +/- 0.02, respectively). We suggest that there is no contraction type-specific control of Ia input to the motoneurons during shortening and lengthening muscle contractions. Cortical adjustments may have occurred.

Adult↗

PubMed1984

Role of calcium in airway smooth muscle contraction and mast cell secretion.

The principal pathological features of asthma, including tracheobronchial smooth muscle contraction and mast cell mediator synthesis and release, are calcium-dependent processes. Calcium plays an integral role in transmitting signals at the cell surface to the enzymatic machinery of the cell interior; its role as the agent for "excitation-contraction coupling" of airway smooth muscle and for "stimulus-secretion coupling" of mast cells is reviewed. A rise in intracellular calcium ion concentration triggers cellular activation. In smooth muscle, calcium bound to calmodulin stimulates the myosin light chain kinase which is important in the regulation of actin-myosin interaction. In mast cells, calcium may bind to calmodulin or to a calmodulinlike regulatory protein, and it also stimulates enzymes important in the synthesis of newly generated mediators including prostaglandins and leukotrienes. The regulatory role of cyclic AMP in both cell systems is discussed, especially as it pertains to calcium metabolism. By interfering with transmembrane calcium fluxes, the calcium channel blocking drugs have the potential for significantly modifying bronchoconstriction and airway inflammation in asthma and related bronchospastic disorders. Some of the in vitro studies of calcium channel blockers in these two cell systems are reviewed. Finally a speculation about the role of abnormal sensitivity to calcium in airway smooth muscle as a potential cause of airway hyperreactivity is entertained.

Asthma↗

PubMed2003

Cardiovascular responses and neurotransmitter changes following blockade of nNOS within the ventrolateral medulla during static muscle contraction.

Nitric oxide (NO) is synthesized from L-arginine through the activity of the synthetic enzyme, NO synthase (NOS). Previous studies have demonstrated the roles of the three isoforms of NOS, namely endothelial NOS (eNOS), neuronal NOS (nNOS), and inducible NOS (iNOS) in cardiovascular regulation. However, no investigation has been done to study their individual role in modulating cardiovascular responses during static skeletal muscle contraction. In this study, we determined the effects of microdialyzing a specific nNOS antagonist into the rostral (RVLM) and caudal ventrolateral medulla (CVLM) on cardiovascular responses and glutamatergic/GABAergic neurotransmission during the exercise pressor reflex using rats. We hypothesized that the NO modulation of the exercise pressor reflex was largely influenced by specific nNOS activity within the ventrolateral medulla. Bilateral microdialysis of a selective nNOS antagonist, 1-(2-trifluoromethylphenyl)-imidazole (1.0 microM), for 30 or 60 min into the RVLM potentiated cardiovascular responses and glutamate release during a static muscle contraction. Levels of GABA within the RVLM were decreased. The cardiovascular responses and neurochemical changes to muscle contraction recovered following discontinuation of the drug. In contrast, bilateral application of the nNOS antagonist into CVLM attenuated cardiovascular responses and glutamate release during a static muscle contraction, but augmented GABA release. These results demonstrate that nNOS in the ventrolateral medulla plays an important role in modulating glutamatergic/GABAergic neurotransmission that regulates the exercise pressor reflex, and contributes to the sympathoexcitatory and sympathoinhibitory actions of NO within the RVLM and CVLM, respectively.

Animals↗

PubMed1997

Central 5-HT1A modulation of cardiovascular responses to tibial nerve stimulation-evoked muscle contraction.

The effects of administering 8-hydroxy-2-(di-n-propylamine) tetralin [8-OH-DPAT, a serotonin 1A (5-HT1A) receptor agonist] into the rostral ventrolateral medulla (RVLM) on cardiovascular responses during tibial nerve stimulation-evoked muscle contraction were investigated using anesthetized rats. Stimulation of the tibial nerve (3 times motor threshold, 0.1 ms, 40 Hz) for 30 s increased mean arterial pressure (MAP), heart rate (HR), and muscle tension by 25 +/- 3 mmHg, 24 +/- 4 beats/min, and 299 +/- 35 g, respectively. Bilateral microdialysis of 8-OH-DPAT (10 mM) for 30 min attenuated the stimulation-evoked increases in MAP (8 +/- 2 mmHg) and HR (11 +/- 5 beats/min), without a change in muscle tension (292 +/- 30 g). However, administration of 1 mM 8-OH-DPAT had no effect on the cardiovascular responses. Thirty minutes of microdialysis of 8-OH-DPAT (10 mM) into the caudal ventrolateral medulla produced no effect on cardiovascular responses during muscle contraction. Prior administration of 10 mM 1-[2-methoxyphenyl]-4-[4-(2-phthalimido)-butyl]piperazine (NAN-190), a 5-HT1A receptor antagonist, for 30 min into the RVLM blocked the attenuating effects of subsequent microdialysis of 8-OH-DPAT (10 mM). Results suggest that activation of 5-HT1A receptors within the RVLM inhibit cardiovascular responses elicited during static muscle contraction.

8-Hydroxy-2-(di-n-propylamino)tetralin↗

PubMed1991

Inflammatory alterations in muscle contraction headache.

To investigate the pathophysiology of muscle contraction headache (MCH), several parameters of inflammation were evaluated in 48 patients suffering from MCH, and compared with 50 healthy control subjects: erythrocyte sedimentation rate; C-reactive protein; white blood cell count; immunoglobulin (Ig) G, A, M; and complement component 3(C3) and C4. Serum C3 and C4 levels were significantly elevated in MCH as compared to control subjects, but the other parameters did not differ significantly. This suggests that the inflammatory process may be involved in the production of MCH.

Adolescent↗