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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↗
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↗
PubMed1991

Optimization of the timing of skeletal to cardiac muscle contraction during dynamic cardiomyoplasty: analysis using a mathematical model.

Cardiomyoplasty, or the use of skeletal muscle to assist the failing heart, has been studied for many years but has enjoyed only minimal success. It has been suggested that a delay in the start of skeletal muscle contraction relative to the QRS complex would enhance aortic flow. To study the effects of simulated changes in the relative timing of skeletal muscle contraction, heart rate and skeletal muscle contraction duration, a mathematical model was used to predict the vascular pressures and flows during cardiomyoplasty. The vascular pressures and cardiac output generated by the model for both the normal and heart failure state were similar to previously published canine data. Skeletal muscle contraction synchronous with cardiac mechanical systole (i.e., delayed approximately 50-75 ms from the QRS) was able to provide improvements in cardiac output, arterial blood pressure and aortic flow velocity up to 40% over the baseline heart failure state. A delay in the start of skeletal muscle contraction, prolonged skeletal muscle contraction duration or an increase in the heart rate from 90 to 120/min reduced this benefit. Thus, mechanical synchrony of skeletal and cardiac muscle contraction optimizes hemodynamics during cardiomyoplasty.

Heart Failure↗
PubMed1979

Early cellular changes and circular muscle contraction associated with the induction of decidualization by intrauterine oil in mice.

Intrauterine instillations of oil or saline distended the uterus in ovariectomized mice treated with progesterone + oestrogen to sensitize the uterus to a decidualizing stimulus. Saline does not induce decidualization, and therefore uterine distension per se is not the trigger to decidual induction. Oil induces decidualization, but does not involve gross damage to the epithelium, penetration of oil into the stroma or release of epithelial lipid into the stroma. Instillation (oil, saline or sham) induced a contraction of the circular muscles along the length of the uterus which closed the uterine lumen, expelled most of the oil and located the remainder primarily in the antimesometrial cleft of the lumen. Progesterone inhibited longitudinal muscle contraction and facilitated circular muscle contraction. These effects are discussed in relation to the spacing and implantation of blastocysts.

Animals↗
PubMedDate not supplied

Cyclosporine does not affect in vitro bronchial smooth muscle contractions in treated Lewis rats.

The purpose of this study was to investigate whether cyclosporine treatment could modify airway responses, thus playing a role in bronchial hyperresponsiveness observed in patients after lung transplantation. We have studied the effect of cyclosporine treatment in rats on subsequent bronchial responses to electrical field stimulation, to exogeneous 5-hydroxytryptamine, and acetylcholine in organ baths. The isometric force of contraction of bronchial smooth muscle was measured. Voltage and frequency responses produced by electrical field stimulation were similar in control and in rat bronchi treated with cyclosporine. Concentration-response curves to exogeneous acetylcholine were superimposed for both groups of animals, as were those to 5-hydroxytryptamine. Our results show that cyclosporine treatment does not affect bronchial smooth muscle contraction and rule out possible contribution of cyclosporine to the bronchial hyperresponsiveness described after lung transplantation.

Acetylcholine↗
PubMed1992

Direct inhibitory mechanisms of halothane on canine tracheal smooth muscle contraction.

Halothane directly relaxes airway smooth muscle. To determine the direct inhibitory mechanisms of halothane on canine tracheal smooth muscle contraction, the effects of this anesthetic on the levels of several intracellular second messengers were investigated by measuring intracellular Ca2+ concentration ([Ca2+]i), Ca2+/phospholipid-dependent protein kinase (PKC) translocation, and intracellular cyclic adenosine monophosphate concentration ([cAMP]i). When carbachol (1 microM) was used to increase [Ca2+]i to the same concentration as that induced by high-K+ (72.7 mM), the carbachol-induced contraction was more than twice as great, indicating that carbachol enhances the sensitivity of contractile elements to Ca2+ or activates a Ca(2+)-independent mechanism. Similarly, 12-deoxyphorbol 13-isobutylate, a potent PKC activator, markedly potentiated high-K(+)-induced muscle contraction without an increase of [Ca2+]i. The addition of halothane (0.33, 0.75, 1.15, and 1.47 mM) decreased [Ca2+]i and the muscle tension induced by carbachol. However, the decrease of muscle tension was more marked than that of [Ca2+]i at the higher concentrations. Although [Ca2+]i in the presence of verapamil and carbachol was not affected by halothane, the anesthetic markedly decreased muscle force by decreasing the "Ca2+ sensitization" or the Ca(2+)-independent enhancement of tension observed with carbachol. Halothane (0.75 and 1.47 mM) significantly released the membrane-associated PKC to cytosol, which decreased PKC activity. [cAMP]i of the smooth muscle stimulated by carbachol was moderately but significantly increased by halothane. However, when equivalent relaxation was induced with forskolin, which acts via adenylate cyclase activation, a much higher [cAMP]i was observed, which suggests that halothane acts via an additional pathway.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

[The manifestation of the hysteresis effects of muscle contraction in the cortically evoked coactivation of muscle antagonists].

Hysteretic after-effects of muscle contraction were studied on unanaesthetized cats during intracortical microstimulation of two sites in the motor cortex. Equilibrium in the joint-external load system was shown to be dependent on the order of stimulation of the sites in the motor cortex. Coactivation of antagonistic muscles led to an increase in both the joint stiffness and uncertainty of the equilibrium value of the joint angle.

Animals↗
PubMed1991

Changes in the baroreceptor reflex at the start of muscle contraction in the decerebrate cat.

1. The action of muscle contraction on the sensitivity of the cardiac vagal component of the baroreceptor reflex was examined in decerebrate cats. 2. The sensitivity of the baroreceptor reflex was expressed as the difference between the maximum prolongation of the R-R interval in response to carotid sinus baroreceptor stimulation and the mean of ten R-R intervals immediately before carotid sinus pressure elevation. 3. Muscle contraction elicited by electrical stimulation of L7 ventral roots (50 Hz) significantly reduced the sensitivity of the baroreceptor reflex by reducing the prolongation of the R-R interval from 269 +/- 31 to 159 +/- 22 ms. 4. Inhibition of the cardiac vagal component of the baroreceptor reflex was seen just 1 s after the onset of contraction and with stimulation frequencies as low as 10 Hz. 5. These results show for the first time that changes in the sensitivity of the baroreceptor reflex during exercise result in part from afferent information originating in the contracting muscles.

Animals↗
PubMed1988

A self-induced translation model of myosin head motion along thin filament in muscle contraction.

Evidence has been accumulating that muscle contraction may not be associated with the power stroke of the cross-bridges tightly coupled with ATP hydrolysis cycle. We have constructed a new contraction model which includes a number of basic properties of contraction processes not taken into consideration in the models hitherto reported. The basic assumption is that, when one head of a myosin molecule attaches to an actin monomer on thin filament, conformational changes take place in the neighbouring actin monomers to result in their non-symmetrical charge distribution to exert electrostatic force on the unattached head of the same myosin molecule in one direction. Thus, the unattached head moves along thin filament to attach to another actin monomer, while the already attached head detaches from thin filament. These steps are repeated to cause muscle contraction. The above contraction model can explain the results of our X-ray diffraction experiments as well as the results reported by other authors.

Actin Cytoskeleton↗
PubMed1991

Excited hydrogen bonds in the molecular mechanism of muscle contraction.

The mechanism of muscle contraction is considered. The hydrolysis of an ATP molecule is assumed to produce the excitation of hydrogen bonds A--H...B between electronegative atoms A and B, which are contained in the myosin head and actin filament. This excitation energy epsilon f depends on the interatomic distance AB = R and generates the tractive force f = -delta epsilon f/delta R, that makes atoms AB approach each other. The swing of the myosin head results in macroscopic mutual displacement of actin and myosin polymers. The motion of the actin filament under the action of this force is studied. The conditions under which a considerable portion of the excitation energy converts into the potential tension energy of the actin filament are analysed, and the probability of higher muscle efficiency existence is discussed.

Actins↗
PubMed1995

Peptidergic innervation of leg muscles of the cockroach, Periplaneta americana (L.), and a possible role in modulation of muscle contraction.

FMRFamide-related peptides of insects are particularly important because of their possible function as neurohormones and neuromodulators on a wide variety of tissues. Part of this study was an investigation of the immunofluorescent staining of motor nerves which arise in the metathoracic ganglion, examined in wholemount using an antiserum that recognizes extended -RFamide peptides (generally recognized to be of the FMRFamide family). This antiserum revealed immunochemical staining of numerous cell bodies in the metathoracic ganglion and of axons in peripheral nerve 5, a large nerve which contains both motor and sensory fibres. Axons staining positive for FMRFamide-related peptides were traced in nerve 5 as far as the femur-tibia joint, and into the first (sensory-motor) and third (motor only) ramus of nerve 5. Reverse-phase HPLC with radioimmunoassay revealed a peak of FMRFamide-related peptide activity in nerve 5 that was coincident with a peak found when thoracic ganglia were processed in the same fashion. A physiological assay was devised to test the ability of various non-native peptides to alter the characteristics of contraction of skeletal muscles of the legs. Using neurally evoked contractions of coxal depressor muscles of the metathoracic leg it was determined that several non-native peptides could potentiate muscle contractions. The results of this study suggest that muscles of the legs receive innervation by identifiable, FMRFamide-related peptide-containing neurons and that the release of peptide(s) at the muscle may be yet another method of modulating the mechanics of muscle contraction.

Animals↗
PubMed1984

Pardaxin produces postjunctional muscle contraction in guinea-pig intestinal smooth muscle.

The action of pardaxin (PX), a toxin isolated from the secretion of the Red Sea flatfish, Pardachirus marmoratus, was studied on longitudinal muscle of guinea-pig ileum. Pardaxin contracted the ileum and subsequently abolished muscle contraction to 5-hydroxytryptamine (5-HT), but did not affect the responses to acetylcholine (ACh) and substance P(SP). Pardaxin-induced contraction was only partially suppressed by atropine and not affected by tetrodotoxin or morphine. Preparations desensitized to 5-HT or SP responded normally to pardaxin. Pardaxin-induced contractions were normal in K+-depolarizing Krebs Ringer solution and not affected by black widow spider venom. It is concluded that the pardaxin-induced muscle contractions are not mediated through the release of neurotransmitters and do not involve 5-HT, SP or ACh receptors, but are due to a direct action on the muscle contractile mechanism.

Acetylcholine↗
PubMed1994

The biochemical basis of the regulation of smooth-muscle contraction.

The primary signal for smooth-muscle contraction is an increase in sarcoplasmic free Ca2+ concentration ([Ca2+]i). This triggers activation of calmodulin-dependent myosin light-chain kinase, which catalyses myosin phosphorylation, thereby activating crossbridge cycling and the development of force or contraction of the muscle cell. Restoration of resting [Ca2+]i deactivates the kinase; myosin is dephosphorylated by myosin light-chain phosphatase and the muscle relaxes. Recent evidence suggests that other signal-transduction pathways can modulate the contractile state of a smooth-muscle cell by affecting specific steps in the myosin phosphorylation-dephosphorylation mechanism.

Animals↗
PubMed1995

Indirect coupling of phosphate release to de novo tension generation during muscle contraction.

A key question in muscle contraction is how tension generation is coupled to the chemistry of the actomyosin ATPase. Biochemical and mechanochemical experiments link tension generation to a change in structure associated with phosphate release. Length-jump and temperature-jump experiments, on the other hand, implicate phase 2slow, a significantly faster, markedly strain-sensitive kinetic process in tension generation. We use a laser temperature jump to probe the kinetics and mechanism of tension generation in skinned rabbit psoas fibers--an appropriate method since both phosphate release and phase 2slow are readily perturbed by temperature. Kinetics characteristic of the structural change associated with phosphate release are observed only when phosphate is added to fibers. When present, it causes a reduction in fiber tension; otherwise, no force is generated when it is perturbed. We therefore exclude this step from tension generation. The kinetics of de novo tension generation by the temperature-jump equivalent of phase 2slow appear unaffected by phosphate binding. We therefore propose that phosphate release is indirectly coupled to de novo tension generation via a steady-state flux through an irreversible step. We conclude that tension generation occurs in the absence of chemical change as the result of an entropy-driven transition between strongly bound crossbridges in the actomyosin-ADP state. The mechanism resembles the operation of a clock, with phosphate release providing the energy to tension the spring, and the irreversible step functions as the escapement mechanism, which is followed in turn by tension generation as the movement of the hands.

Actomyosin↗