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PubMed1994

Calcium and smooth muscle contraction.

The fact that smooth muscle exists in almost every hollow organ and is involved in a large number of disease states has led to a vast increase in smooth muscle research, covering areas from testing response to antagonists and agonists to measuring the molecular force generated by a single actin filament. Yet, the exact mechanisms regulating contractile response of smooth muscle remain unsolved. Calcium has been a central player in mediating smooth muscle contraction through binding with calmodulin, although there is evidence showing that under special circumstances smooth muscle can contract without change in intracellular Ca2+. In addition to the major regulatory pathway of Ca(2+)-calmodulin-myosin light chain kinase, there are other thin filament linked regulatory mechanisms in which Ca(2+)-calmodulin dependent phosphorylation of calponin and caldesmon may be involved. Ca2+ sensitivity of smooth muscle contraction may vary under different situations and this has recently been recognized as an important regulatory mechanism. Examples are protein kinase C (PKC) dependent phosphorylation of myosin light chain kinase which results in partial inhibition of contraction, and activation of myosin light chain phosphatase. There is new evidence showing that not only does Ca2+ regulate contraction by regulating the interaction of contractile proteins in smooth muscle, but also that shortening of smooth muscle itself reduces intracellular Ca2+ concentration, via a negative feedback.

Actins↗

PubMed2005

Dynamics of myosin-driven skeletal muscle contraction: I. Steady-state force generation.

Skeletal muscle contraction is a canonical example of motor-driven force generation. Despite the long history of research in this topic, a mechanistic explanation of the collective myosin force generation is lacking. We present a theoretical model of muscle contraction based on the conformational movements of individual myosins and experimentally measured chemical rate constants. Detailed mechanics of the myosin motor and the geometry of the sarcomere are taken into account. Two possible scenarios of force generation are examined. We find only one of the scenarios can give rise to a plausible contraction mechanism. We propose that the synchrony in muscle contraction is due to a force-dependent ADP release step. Computational results of a half sarcomere with 150 myosin heads can explain the experimentally measured force-velocity relationship and efficiency data. We predict that the number of working myosin motors increases as the load force is increased, thus showing synchrony among myosin motors during muscle contraction. We also find that titin molecules anchoring the thick filament are passive force generators in assisting muscle contraction.

Adenosine Diphosphate↗

PubMed2003

Sustained muscle contractions maintained by autonomous neuronal activity within the human spinal cord.

It is well known that muscle contraction can be easily evoked in the human soleus muscle by applying single-pulse electrical stimulation to the tibial nerve at the popliteal fossa. We herein reveal the unexpected phenomenon of muscle contractions that can be observed when train stimulation is used instead. We found, in 11 human subjects, that transient electrical train stimulation (1-ms pulses, 50 Hz, 2 s) was able to induce sustained muscle contractions in the soleus muscle that outlasted the stimulation period for greater than 1 min. Subjects were unaware of their own muscle activity, suggesting that this is an involuntary muscle contraction. In fact, the excitability of the primary motor cortex (M1) with the sustained muscle contractions evaluated by transcranial magnetic stimulation was lower than the excitability with voluntary muscle contractions even when both muscle contraction levels were matched. This finding indicates that M1 was less involved in maintaining the muscle contractions. Furthermore, the muscle contractions did not come from spontaneous activity of muscle fibers or from reverberating activity within closed neuronal circuits involving motoneurons. These conclusions were made based on the respective evidence: 1) the electromyographic activity was inhibited by stimulation of the common peroneal nerve that has inhibitory connections to the soleus motoneuron pool and 2) it was not abolished after stopping the reverberation (if any) for approximately 100 ms by inducing the silent period that followed an H-reflex. These findings indicate that the sustained muscle contractions induced in this study are most likely to be maintained by autonomous activity of motoneurons and/or interneurons within the human spinal cord.

Adult↗

PubMed1994

[Studies on agonists and antagonists of smooth muscle contraction by the use of an actomyosin preparation].

The sites of action of many chemical agents that modify the contraction of smooth muscle are in the smooth muscle membrane. However, a few agents, such as calmodulin inhibitors and protein kinase inhibitors, interact directly with contractile elements of the actomyosin system so as to modify smooth muscle contraction. Here, we describe experimental procedures that are applicable for the screening of smooth muscle relaxants with this mode of action. Myosin B was extracted from chicken gizzard smooth muscle. Because myosin B was a crude preparation of smooth muscle actomyosin, it consisted of regulatory proteins of calmodulin, myosin light chain kinase and protein phosphatase in addition to the contractile proteins of actin and myosin. Interaction of chemical agents with these proteins could be detected by measuring the Mg-ATPase activity of the myosin B preparation. Then we examined whether the agents that altered the ATPase activity was associated with changes in phosphorylation of myosin light chain. If the levels are altered, the agents may interact with the regulatory protein(s). If not, the site of their action was in the contractile proteins. The analysis with these respective proteins will be also described.

Amiloride↗

PubMed2001

Involvement of phosphorylation of myosin phosphatase by ROCK in trabecular meshwork and ciliary muscle contraction.

The control of smooth muscle contraction is an important factor in maintaining normal intraocular pressure. However, the specific factors causing changes in control by phosphorylation/dephosphorylation schemes in the eye are not well-defined. The purposes of this experiment were to (i) determine the localization of ROCK (Rho-associated, coiled coil-forming kinase) in monkey and rabbit eye tissues and (ii) measure phosphorylation of ROCK substrate during trabecular meshwork or ciliary muscle contraction induced by carbachol. We found that mRNAs for both ROCK I and II were expressed in most eye tissues from rabbit and monkey. Proteins for ROCK I and II were present in all eye tissues studied except lens. When trabecular meshwork or ciliary muscle were incubated with carbachol to induce contraction, phosphorylation of the myosin-binding subunit (MBS) of myosin phosphatase, a substrate for ROCK, started within 1 min and continued for at least 1 h. This phosphorylation was well correlated with contraction of trabecular meshwork or ciliary muscle. These results suggested that ROCK might regulate contraction of trabecular meshwork or ciliary muscle through phosphorylation of MBS of myosin phosphatase.

Animals↗

PubMed1999

Cardiovascular responses to muscle contraction following microdialysis of nitric oxide precursor into ventrolateral medulla.

We determined the effects of administering L-arginine, a precursor for the synthesis of nitric oxide, and L-NMMA (NG-monomethyl-L-arginine), a nitric oxide synthase blocker, into the rostral (RVLM) and caudal (CVLM) ventrolateral medulla on cardiovascular responses elicited during static contraction of the triceps surae muscle. Two microdialysis probes were inserted bilaterally into the RVLM or CVLM of anesthetized Sprague-Dawley rats using stereotaxic guides. For RVLM experiments, static muscle contraction evoked by stimulation of the tibial nerve increased mean arterial pressure (MAP) and heart rate (HR) by 29+/-3 mmHg and 44+/-7 bpm, respectively (n=8). Microdialysis of L-arginine (1.0 microM) for 30 min attenuated the contraction-evoked increases in MAP and HR. After discontinuing L-arginine, L-NMMA (1.0 microM) was microdialyzed into the RVLM for an additional 30 min followed by a muscle contraction. This contraction augmented the pressor response (37+/-4 mmHg) and HR (61+/-11 bpm) with respect to control values. For CVLM experiments, muscle contraction increased MAP and HR by 23+/-3 mmHg and 25+/-5 bpm, respectively (n=9). Microdialysis of L-arginine (1.0 microM) for 30 min potentiated the contraction-evoked increases in MAP and HR. Subsequent administration of L-NMMA (1.0 microM) into the CVLM for an additional 30 min blocked the augmented MAP and HR responses. Developed tensions did not alter during contractions throughout both RVLM and CVLM protocols. These results suggest that nitric oxide, within the RVLM and CVLM, plays an opposing role in modulating cardiovascular responses during static muscle contraction.

Animals↗

PubMed1991

The Ayerst Award Lecture 1990. Calcium-dependent mechanisms of regulation of smooth muscle contraction.

The contractile state of smooth muscle is regulated primarily by the sarcoplasmic (cytosolic) free Ca2+ concentration. A variety of stimuli that induce smooth muscle contraction (e.g., membrane depolarization, alpha-adrenergic and muscarinic agonists) trigger an increase in sarcoplasmic free [Ca2+] from resting levels of 120-270 to 500-700 nM. At the elevated [Ca2+], Ca2+ binds to calmodulin, the ubiquitous and multifunctional Ca(2+)-binding protein. The interaction of Ca2+ with CaM induces a conformational change in the Ca(2+)-binding protein with exposure of a site(s) of interaction with target proteins, the most important of which in the context of smooth muscle contraction is the enzyme myosin light chain kinase. The interaction of calmodulin with myosin light chain kinase results in activation of the kinase that catalyzes phosphorylation of myosin at serine-19 of each of the two 20-kDa light chains (native myosin is a hexamer composed of two heavy chains (230 kDa each) and two pairs of light chains (one pair of 20 kDa each and the other pair of 17 kDa each)). This simple phosphorylation reaction triggers cycling of myosin cross-bridges along actin filaments and the development of force. Relaxation of the muscle follows removal of Ca2+ from the sarcoplasm, whereupon calmodulin dissociates from myosin light chain kinase regenerating the inactive kinase; myosin is dephosphorylated by myosin light chain phosphatase(s), whereupon it dissociates and remains detached from the actin filament and the muscle relaxes. A substantial body of evidence has been accumulated in support of this central role of myosin phosphorylation-dephosphorylation in the regulation of smooth muscle contraction. However, a wide range of physiological and biochemical studies supports the existence of additional, secondary Ca(2+)-dependent mechanisms that can modulate or fine-tune the contractile state of the smooth muscle cell. Three such mechanisms have emerged: (i) the actin-, tropomyosin-, and calmodulin-binding protein, calponin; (ii) the actin-, myosin-, tropomyosin-, and calmodulin-binding protein, caldesmon; and (iii) the Ca(2+)- and phospholipid-dependent protein kinase (protein kinase C).

Actin Cytoskeleton↗

PubMed1994

The effects of muscle contraction and insulin on glucose-transporter translocation in rat skeletal muscle.

The effect of electrically induced muscle contraction, insulin (10 m-units/ml) and electrically-induced muscle contraction in the presence of insulin on insulin-regulatable glucose-transporter (GLUT-4) protein distribution was studied in female Sprague-Dawley rats during hindlimb perfusion. Plasma-membrane cytochalasin B binding increased approximately 2-fold, whereas GLUT-4 protein concentration increased approximately 1.5-fold above control with contractions, insulin, or insulin + contraction. Microsomal-membrane cytochalasin B binding and GLUT-4 protein concentration decreased by approx. 30% with insulin or insulin + contraction, but did not significantly decrease with contraction alone. The rate of muscle glucose uptake was assessed by determining the rate of 2-deoxy[3H]glucose accumulation in the soleus, plantaris, and red and white portions of the gastrocnemius. Both contraction and insulin increased glucose uptake significantly and to the same degree in the muscles examined. Insulin + contraction increased glucose uptake above that of insulin or contraction alone, but this effect was only statistically significant in the soleus, plantaris and white gastrocnemius. The combined effects of insulin + contraction of glucose uptake were not fully additive in any of the muscles investigated. These results suggest that (1) insulin and muscle contraction are mobilizing two separate pools of GLUT-4 protein, and (2) the increase in skeletal-muscle glucose uptake due to insulin + contraction is not due to an increase in plasma-membrane GLUT-4 protein concentration above that observed for insulin or contraction alone.

Animals↗

PubMed1996

Excitatory amino acid concentrations in the spinal dorsal horn of cats during muscle contraction.

In anesthetized cats, static hindlimb muscle contraction reflexly increases mean arterial pressure (MAP) and heart rate (HR). Pharmacological and immunohistochemical evidence suggests that excitatory amino acids are involved in the spinal transmission of this reflex. Using microdialysis and high-performance liquid chromatography technology, we tested the hypothesis that static contraction of the triceps surae muscle increases the extracellular concentration of glutamate (Glu) and aspartate (Asp) at the L7 level of the dorsal horn of the spinal cord. With the exception of the L7 dorsal root, the L5-S2 dorsal and ventral roots were cut ipsilateral to the contracting muscle. After the insertion of microdialysis probes and a 3-h recovery period, a 2-min static contraction was electrically evoked. MAP and HR increased by 53 +/- 8 mmHg and 20 +/- 4 beats/min. The concentration of Glu increased from 324 +/- 59 to 857 +/- 80 nM, whereas Asp increased from 199 +/- 57 to 499 +/- 113 nM. These results were repeatable, in that Glu and Asp rose by similar amounts in two subsequent contractions. In both of these latter contractions, MAP and HR were also significantly increased. By contrast, in a subset of cats whose L7 dorsal roots were cut after the first contraction, neither MAP, HR, Glu, nor Asp was significantly increased over baseline levels. These data demonstrate that static contraction of the hindlimb increases the extracellular concentration of Glu and Asp in the dorsal horn. In summary, the results from this study are in agreement with previous findings suggesting that excitatory amino acids are involved in the spinal transmission of sensory information from the hindlimb muscle.

Animals↗

PubMedDate not supplied

[Kinetic model of a single muscle contraction].

A model of single muscle contraction is proposed. The kinetics of two reactions have been used: interaction between the excitation mediator and the muscle membrane receptor, and the reaction of enzymatic mediator splitting. The muscle contraction parameters have been correlated with the concentration of the mediator-receptor complex.

Kinetics↗

PubMed2007

In vivo myograph measurement of muscle contraction at optimal length.

BACKGROUND: Current devices for measuring muscle contraction in vivo have limited accuracy in establishing and re-establishing the optimum muscle length. They are variable in the reproducibility to determine the muscle contraction at this length, and often do not maintain precise conditions during the examination. Consequently, for clinical testing only semi-quantitative methods have been used. METHODS: We present a newly developed myograph, an accurate measuring device for muscle contraction, consisting of three elements. Firstly, an element for adjusting the axle of the device and the physiological axis of muscle contraction; secondly, an element to accurately position and reposition the extremity of the muscle; and thirdly, an element for the progressive pre-stretching and isometric locking of the target muscle. Thus it is possible to examine individual in vivo muscles in every pre-stretched, specified position, to maintain constant muscle-length conditions, and to accurately re-establish the conditions of the measurement process at later sessions. RESULTS: In a sequence of experiments the force of contraction of the muscle at differing stretching lengths were recorded and the forces determined. The optimum muscle length for maximal force of contraction was established. In a following sequence of experiments with smaller graduations around this optimal stretching length an increasingly accurate optimum muscle length for maximal force of contraction was determined. This optimum length was also accurately re-established at later sessions. CONCLUSION: We have introduced a new technical solution for valid, reproducible in vivo force measurements on every possible point of the stretching curve. Thus it should be possible to study the muscle contraction in vivo to the same level of accuracy as is achieved in tests with in vitro organ preparations.

Equipment Design↗

PubMed2003

Direct demonstration of reduction of the output of the human motor cortex induced by a fatiguing muscle contraction.

A brief period of strong muscle contraction suppresses the amplitude of EMG responses evoked in relaxed muscle by transcranial magnetic stimulation (TMS) of the contralateral motor cortex. Here we investigate this phenomenon in more detail by recording the descending motor volleys evoked by TMS from electrodes in the cervical epidural space of three conscious patients implanted with chronic electrical stimulators for control of pain. We confirm that fatigue suppresses I waves evoked by TMS. In addition, D waves were suppressed in two of the patients, suggesting that axonal excitability might also be compromised by a period of intense muscle contraction.

Adult↗

PubMed1994

Role of intracellular Ca2+ pools in the effects of halothane and isoflurane on vascular smooth muscle contraction.

We examined the effect of halothane and isoflurane on contraction in the vascular smooth muscle of rat thoracic aorta simultaneously with the cytosolic Ca2+ levels ([Ca2+]i). Isolated spiral strips of rat thoracic aorta were suspended for isometric tension recordings in physiologic salt solution. The [Ca2+]i was measured concomitantly using fura-2-Ca2+ fluorescence. Muscle tension was elicited either by 51 mM K+ solution or 30 nM norepinephrine, and the muscle was exposed to 0%, 1%, 2%, 3% halothane or 0%, 1%, 2%, 3%, 4% isoflurane. The effects of the anesthetics were compared with the effects of verapamil, an L-type voltage-dependent Ca2+ channel blocker, also administered during K(+)-induced muscle contraction. In another series, the effects of the anesthetics on caffeine- or norepinephrine-induced muscle contraction were determined in Ca(2+)-free solution. Finally, 3% halothane or 4% isoflurane was administered during K(+)-induced contraction in muscle strips pretreated with ryanodine and caffeine. During K(+)-induced contraction, halothane evoked a transient increase followed by a decrease in both muscle tension and [Ca2+]i. The biphasic change in muscle tension was not elicited by isoflurane or by any agent under norepinephrine-induced contraction. Both halothane and isoflurane ultimately suppressed both K(+)- and norepinephrine-induced increases in muscle tension and the [Ca2+]i in a concentration-dependent manner. The slopes of the [Ca2+]i-tension regression lines under the two anesthetics were significantly steeper than that under verapamil during K(+)-induced contraction. Halothane, but not isoflurane, augmented 4 mM caffeine-induced tension and [Ca2+]i transients in the Ca(2+)-free solution in a concentration-dependent manner. However, neither anesthetic influenced norepinephrine-induced tension and [Ca2+]i transients. In the muscle strips pretreated with ryanodine and caffeine, the difference observed between the anesthetics was abolished. In conclusion, halothane, but not isoflurane, enhances Ca2+ release predominantly from the caffeine-releasable Ca2+ stores in vascular smooth muscle; this release may modify the effect of halothane. The intracellular Ca2+ pools can be affected differently by volatile anesthetic drugs, depending on the nature of the stimulus for smooth muscle contraction.

Animals↗

PubMed1987

Protein kinase C in the regulation of smooth muscle contraction.

The cellular and molecular mechanisms underlying smooth muscle contraction are reviewed in the light of recent studies of smooth muscle ultrastructure and of the role of polyphosphoinositide turnover and protein kinase C function in smooth muscle contraction. A new model of smooth muscle contraction is proposed that differs radically from accepted views, particularly the latch bridge hypothesis, in terms of both Ca2+ messenger function and the molecular events underlying this process. A coordinate fibrillar domain model of contraction is proposed in which the initial and sustained phases of contraction are mediated by different cellular and molecular events. The initial phase of response is mediated by a rise in [Ca2+]c and the resulting calmodulin-dependent activation of both myosin light chain kinase and the dissociation of caldesmon from the actin-caldesmon-tropomyosin-myosin fibrillar domain. These events lead to an interaction between actin and the phosphorylated light chains of myosin just as in previous models. However, this initial phase is followed by a sustained phase in which a rise in [Ca2+]sm stimulates the plasma membrane-associated, Ca2+-sensitive form of protein kinase C that results in the phosphorylation of both structural and regulatory components of the filamin-actin-desmin fibrillar domain. These events underlie the tonic phase of contraction.

Adenosine Triphosphatases↗

PubMed2001

Spontaneously hypertensive rats exhibit altered cardiovascular and neuronal responses to muscle contraction.

We examined the cardiovascular and ventrolateral medullary neuronal responses to muscle contraction in the spontaneously hypertensive rat (SHR) and normotensive Wistar-Kyoto rat (WKY) control. Cardiovascular, respiratory and ventrolateral medullary neuronal responses to muscle contraction evoked by tibial nerve stimulation were recorded. SHRs exhibited significantly larger drops in arterial pressure compared to WKYs in response to muscle contraction (P < 0.05). Basal ventrolateral medulla neuronal discharge rates were similar between the SHR and the WKY groups. A majority of neurons recorded responded to muscle contraction in both the WKY (77 %; n = 53) and the SHR groups (68 %; n = 62). There was no difference in the percentage of neurons that responded with an increase (approximately 60 %) or decrease (approximately 40 %) in firing rate between hypertensive and normotensive rats. Pulse wave-triggered averaging techniques showed that most neurons that responded to muscle contraction also possessed a basal firing rhythm temporally related to the cardiac cycle (85 % in WKYs, 83 % in SHRs). However, decreases in neuronal firing rates in response to muscle contraction were significantly greater in SHRs than WKYs. Therefore, we conclude that muscle contraction unmasks a hyperexcitability of neurons in the ventrolateral medulla of SHRs that parallels the heightened blood pressure responses.

Animals↗

PubMed1993

The influence of muscle contraction on the degree of microvascular perfusion in rat skeletal muscle following transcutaneous neuromuscular electrical stimulation.

Electrotherapy is used clinically according to a variety of protocols and at various intensities with the intent of effecting any number of physiological changes. The purpose of this study was to determine if the increased degree of microvascular perfusion observed following 2,500 Hz transcutaneous neuromuscular electrical stimulation (TNMES) is dependent on evoked muscle contractions. The tibialis anterior (TA) and extensor digitorum longus (EDL) muscles from 30 male rats were analyzed. Six animals were untreated and served as controls, while the TA and EDL muscles of six animals were treated with TNMES at current intensities three times that needed to evoke a minimum visible contraction in the TA (M-TNMES). The remaining animals were treated with gallamine, which effectively blocked neurally mediated muscle contraction. The TA and EDL muscles of six gallamine-treated rats received no TNMES and served as shams (G-Sham), six received M-TNMES (GM-TNMES), and six received TNMES at intensities sufficient to produce sustained muscle contraction with a neuromuscular blockade in place (G-HIS). Perfused microvessels were labeled with fluorescein isothiocyanate-bovine serum albumin. The degree of microvascular perfusion was determined by calculating perfused microvessel/muscle fiber ratios (PV/F). The mean PV/F ratios of all groups were compared using Fisher's LSD (alpha = 0.05). When compared to controls, the PV/F ratios of the TA and EDL muscles in M-TNMES and G-HIS groups showed a significant (p < or = 0.05) increase while the G-Sham and GM-TNMES groups were similar to controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗

PubMed1987

Natriuretic and smooth muscle contracting activities isolated from human urine.

Human urine contains a small molecular weight natriuretic substance and similar material isolated from the kidney inhibits Na/K ATPase. Such action on blood vessels would cause contraction. Human urinary natriuretic material isolated from a Sephadex G-25 column contracted smooth muscle in the rat anococcygeus muscle. Known vasoactive substances could not explain the activity of the natriuretic fraction on the anococcygeus muscle. In subsequent studies the natriuretic fraction from the Sephadex G-25 column was run on a Sephadex G-10 column and natriuretic activity was found before the sodium was eluted. The same fractions inhibited Na/K ATPase but did not cause contraction of the anococcygeus muscle. The fractions which did cause contraction of the anococcygeus muscle were eluted long after the salts and these fractions did not inhibit Na/K ATPase and were not natriuretic. The postulated defect in sodium excretion in hypertensive patients might be related to their low kallikrein excretion. Since ANP stimulates increased kallikrein release in rats and does not inhibit Na/K ATPase, it is suggested that the natriuretic pathway via inhibition of renal Na/K ATPase is independent in the kidney of the kallikrein/kinin natriuretic pathway.

Animals↗

PubMed1969

Activation in a skeletal muscle contraction model with a modification for insect fibrillar muscle.

A sliding filament model for muscle contraction is extended by including an activation mechanism based on the hypothesis that the binding of calcium by a regulating protein in the myofibrils must occur before the rate constant governing the making of interactions between cross-bridges and thin filament sites can take on nonzero values. The magnitude of the rate constant is proportional to the amount of bound calcium. The model's isometric twitch and rise of force in an isometric tetanus are similar to the curves produced by real muscles. It redevelops force after a quick release in an isometric tetanus faster than the initial rise. Quick release experiments on the model during an isometric twitch show that the "active state" curve produced is different from the postulated calcium binding curve. The force developed by the model can be increased by a small quick stretch delivered soon after activation to values near the maximum generated in an isometric tetanus. Following the quick stretch, the force remains near the tetanic maximum for a long time even though the calcium binding curve rises to a peak and subsequently decays by about 50%. The model satisfies the constraint of shortening with a constant velocity under a constant load. Modifications can be made in the model so that it produces the delayed force changes following step length changes characteristic of insect fibrillar muscle.

Animals↗