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PubMed1991

Regulation of a smooth muscle contraction: a hypothesis based on skinned fiber studies.

It seems clear that a simple Ca2+ dependent switch (MLC phosphorylation) cannot completely explain all of the disparate mechanical and energetic results obtained under numerous experimental conditions in numerous laboratories. Some of the problems of the simple switch model are that: 1. Force can be developed in the complete absence of increases in MLC phosphorylation; 2. Crossbridge cycling rate, as measured by either shortening velocity or directly by ATPase activity, can be regulated independent of changes in MLC phosphorylation; and 3. Ca2+ can directly influence both force and crossbridge cycling rate. Thus, we believe that there are two distinct Ca2+ dependent regulatory systems which normally act in parallel to contract smooth muscle. One of these is the Ca2+ dependent MLC phosphorylation-dephosphorylation. system which is likely to be responsible for the rapid development of force. The other is the hypothesized Ca2+ dependent system which is probably responsible for the slow development of force as well as the maintenance of previously developed force, represented in Figure 5 as K8. This second system involves a calmodulin-like protein with a higher Ca2+ sensitivity than that for the Ca(2+)-calmodulin-MLC kinase system. Under most conditions, the total force attained by smooth muscle in response to stimulation is the result of the concerted activation of both of these regulatory systems. The available information is consistent with this hypothesis of two regulatory systems functioning in parallel. In addition to the information presented in this chapter, work from a number of laboratories (Moreland and Ford, 1982; Fujiwara et al., 1989; Kitazawa et al., 1989; Somlyo et al., 1989; Kubota et al., 1990; Kitazawa and Somlyo, this volume) have suggested the possibility that a regulated MLC phosphatase may functionally alter the Ca2+ sensitivity of the contractile filaments. There is evidence suggesting that the sensitivity of MLC kinase to activation by Ca2+ and calmodulin may be regulated (Stull et al., this volume). Protein kinase C has been postulated to play an important role in the regulation of myofilament Ca2+ sensitivity (Nishimura et al., this volume). MgADP has been suggested to affect the kinetics of latchbridge attachment and detachment (Kerrick and Hoar, 1987; Nishimura and van Breemen, 1989). Cooperativity between crossbridges as described by Somlyo et al. (1988) and Siegman et al. (this volume) might also be an important component in the regulation of smooth muscle contraction.(ABSTRACT TRUNCATED AT 400 WORDS)

Animals↗
PubMed1986

Surgical sympathetic denervation increases alpha 1-adrenoceptor-mediated accumulation of myo-inositol trisphosphate and muscle contraction in rabbit iris dilator smooth muscle.

Sympathetic denervation of the iris muscle produces increases in both the breakdown of phosphatidylinositol 4,5-bisphosphate (PIP2) and in muscle contraction in response to norepinephrine (NE). To shed more light on the biochemical basis underlying this supersensitivity we investigated: the effects of NE on PIP2 breakdown, measured as myo-inositol trisphosphate (IP3) accumulation, and on muscle contraction in normal and denervated rabbit iris dilator; and the effects of denervation on selected biochemical properties of this muscle. The data obtained from these studies can be summarized as follows: The EC50 values (microM) for NE-induced IP3 accumulation in normal and denervated dilators were 14 and 3, respectively. This accumulation of IP3 was blocked by prazosin (1 microM). The EC50 values (microM) for NE-induced contraction for the normal and denervated muscles were 10 and 0.6, respectively. The NE-induced muscle contraction was blocked by prazosin (1 microM). The t1/2 values (s) for IP3 accumulation in normal and denervated muscles were 31 and 11, respectively, and for contraction the values were 19 and 9, respectively. Denervation increased significantly (15-18%) the basal labelling of phosphoinositides from myo-[3H]inositol, but not from 32P or [14C]arachidonic acid. Denervation had little effect on the activities of the enzymes involved in phosphoinositide metabolism. However, the activities of protein kinase C and Ca2+-ATPase increased in the denervated muscle. It is concluded that sympathetic denervation of the iris dilator renders the coupling between alpha1 receptors and PIP2 breakdown into IP3 and 1,2-diacylglycerol (DG) more efficient.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine Triphosphatases↗
PubMed1983

Loss of Ca2+-dependent regulation in glycerinated skeletal muscle contraction.

Glycerinated muscle fiber from rabbit psoas muscle often lost Ca2+-dependent regulation of its contraction with long-term extraction in a 50% glycerol solution containing 5 mM EGTA at -20 degrees C, designated as Ca2+-insensitive muscle fiber (CaIS-fiber). About 30 or 40% of glycerinated muscle fibers were CaIS-fibers after 1 to 3 months in the glycerol solution. We investigated the cause of the loss of Ca2+-sensitivity of the glycerinated muscle fiber by tension mechanogram and SDS polyacrylamide gel electrophoresis. This natural CaIS-fiber showed a new band of 30K daltons peptide on SDS gels. On the other hand, Ca2+-sensitive fiber (CaS-fiber) changed to CaIS-fiber by trypsin digestion for 40 sec. The tryptic CaIS-fiber had no troponin C and 30K daltons peptide bands in the electrophoretograms. Incubating with 2 mM CaCl2 for 40 hr at 25 degrees C, CaS-fiber changed easily to CaIS-fiber which had 30K daltons peptide and faint troponin T and I bands, as in natural CaIS-fiber. All CaIS-fibers could recover their Ca2+-dependent regulation by incubating with native tropomyosin from rabbit skeletal muscle for 2 days at 4 degrees C. These results indicate that the loss of Ca2+-dependent regulation of glycerinated muscle fiber is due to degradation of regulatory protein system by endogenous Ca2+-activated proteolytic enzymes.

Animals↗
PubMed1996

Thromboxane A2 antagonist inhibits leukotriene D4-induced smooth muscle contraction in guinea-pig lung parenchyma, but not in trachea.

Although the bronchoconstriction induced by leukotriene D4 (LTD4) has been reported to be partly mediated by thromboxane A2 (TXA2) in the guinea-pig airway, it is not known which part of the airway is susceptible to TXA2. In order to determine the role of TXA2 in the central and peripheral airways, we compared the effect of a TXA2 antagonist on tracheal strips to its effect on parenchymal strips of guinea-pigs. Tracheal and parenchymal strips were mounted in a 3.5 ml organ bath filled with Krebs-Henseleit solution aerated with 95% O2, 5% CO2 and kept at 37 degrees C. After equilibration for 60 min in Krebs solution, the strip was contracted by exposure to 10(-5) M of acetylcholine (ACh). Sixty minutes after ACh was eliminated, the concentration-response curve to LTD4 (10(-9) M-10(-7) M) was obtained, and the LTD4-induced contractions were expressed as the percent of the contraction evoked by 10(-5) M of ACh. We measured the contractile response to LTD4 in the presence or absence of the TXA2 antagonist, BAY u3405 (10(-8) M-10(-6) M). In the tracheal strips, BAY u3405 had no effect on the LTD4-induced contraction. However, in parenchymal strips, BAY u3405 significantly suppressed the contractile response to LTD4. These results suggest that in the central airway LTD4 contracts smooth muscle directly, but that in the peripheral airway LTD4 induces smooth muscle contraction both directly and indirectly, via TXA2.

Animals↗
PubMed1997

Muscle contraction and fatigue. The role of adenosine 5'-diphosphate and inorganic phosphate.

Though many explanations are offered for the fatigue process in contracting skeletal muscle (both central and peripheral factors), none completely explain the decline in force production capability because fatigue is specific to the activity being performed. However, one needs to look no further than the muscle contraction crossbridge cycle itself in order to explain a major contributor to the fatigue process in exercise of any duration. The byproducts of adenosine 5'-triphosphate (ATP) hydrolysis, adenosine 5'-diphosphate (ADP) and inorganic phosphate (Pi) are released during the crossbridge cycle and can be implicated in the fatigue process due to the requirement of their release for proper crossbridge activity. Pi release is coupled to the powerstroke of the crossbridge cycle. The accumulation of Pi during exercise would lead to a reversal of its release step, therefore causing a decrement in force production capability. Due to the release of Pi with both the immediate (phosphagen) energy system and the hydrolysis of ATP, Pi accumulation is probably the largest contributor to the fatigue process in exercise of any duration. ADP release occurs near the end of the crossbridge cycle and therefore controls the velocity of crossbridge detachment. Therefore, ADP accumulation, which occurs during exercise of extended duration (or in ischaemic conditions), causes a slowing of the rate constants (and therefore a decrease in the maximal velocity of shortening). in the crossbridge cycle and a reduced oscillatory power output. The combined effects of these accumulated hydrolysis byproducts accounts for a large amount of the fatigue process in exercise of any intensity or duration.

Adaptation, Physiological↗
PubMed1999

CD4 T cells and major histocompatibility complex class II expression influence worm expulsion and increased intestinal muscle contraction during Trichinella spiralis infection.

Expulsion of intestinal nematode parasites and the associated increased contraction by intestinal muscle are T cell dependent, since both are attenuated in athymic rodents. The CD4 T-cell subset has been strongly associated with worm expulsion; however, the relationship between these cells, antigen presentation, and worm expulsion is not definitive and the role of these factors in intestinal muscle hypercontractility has not been defined. We infected C57BL/6, athymic, CD4-deficient, CD8alpha-deficient, and major histocompatibility complex class II (MHC II)-deficient (C2d) mice with Trichinella spiralis larvae. We examined intestinal worm numbers, longitudinal muscle contraction, and MHC II expression. Numerous MHC II-positive cells were identified within the muscularis externa of infected but not uninfected C57BL/6 mice. C57BL/6 and CD8alpha-deficient mice developed large increases in muscle contraction, expelling the parasite by day 21. Athymic and C2d mice exhibited much smaller increases in muscle contraction and delayed parasite expulsion. CD4-deficient mice exhibited intermediate levels of muscle contraction and delayed parasite expulsion. To further examine the role of MHC II and CD4 T cells, we irradiated C2d mice and reconstituted them with C57BL/6 bone marrow alone or with C57BL/6 CD4 T cells. C57BL/6 bone marrow alone did not affect muscle function or worm expulsion in recipient C2d mice. Partial CD4 T-cell reconstitution was sufficient to restore increased muscle contraction but not worm expulsion. Thus, hematopoietic MHC II expression alone is insufficient for the development of muscle hypercontractility and worm expulsion, but the addition of even small numbers of CD4 T cells was sufficient to induce intestinal muscle pathophysiology.

Animals↗
PubMed1985

Calcium-dependent muscle contraction in obliquely striated Ascaris suum muscle.

The regulatory proteins of Ascaris suum striated skeletal muscle were partially purified and characterized. A tropomyosin isoform (Mr 41K) and three troponin subunits identified as troponin T (Mr 37.5K), troponin I (Mr 25.5K) and troponin C (Mr 18.5K) were purified. Three myosin light chains (Mr 25K, 19K, and 17K) were isolated from washed Ascaris actomyosin; the 19K subunit was phosphorylated in vitro. A calcium/calmodulin-dependent myosin light chain kinase activity was identified in the muscle. In contrast to previously reported data suggesting that Ascaris obliquely striated muscle contraction is regulated by a myosin-mediated mechanism, these data indicate that all of the proteins required for actin-mediated, calcium-dependent muscle contraction are present in this tissue.

Animals↗
PubMed1990

[Significance of flexed posture and neck instability as a cause of chronic muscle contraction headache].

Cause of a muscle contraction headache (MCH) is due to sustained contraction of the neck and head muscles. This is proved by the effect of local anesthesia and EMG findings. However, the pathophysiology of abnormal muscle contraction is still unclear. Also, there is no explanation about female's greater susceptibility to MCH. The purpose of our report is to study the mechanism of abnormal muscle contraction and to find out a way to prevent it. We have examined 826 (572 female & 254 male) patients with MCH using EMG and dynamic X-ray. Results are most of MCH patients have a tendency to bend their head downward at the onset of headache. EMG shows continuous discharge of the posterior neck muscles so long as they keep this posture. Once they look up, however, EMG discharge usually subsides. Therefore, these muscle contraction are not involuntary, but passive as the results of drooping head. In 12 patients, severe attack of MCH were temporarily alleviated by the local anesthesia to the suboccipital tender point. In patients complaining MCH of one side, they often have a tendency to bend their neck toward the opposite direction, thus contracting the painful side of the neck muscles. It is also found that looking up to make orbito-meatal line more than 10 degrees from horizontal plane is enough to minimize muscle contraction, and to prevent or alleviate headache. Not all people experience headache, though.(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed2002

Activation of spinobulbar lamina I neurons by static muscle contraction.

Spinal lamina I neurons are selectively activated by small-diameter somatic afferents, and they project to brain stem sites that are critical for homeostatic control. Because small-diameter afferent activity evoked by contraction of skeletal muscle reflexly elicits exercise-related cardiorespiratory activation, we tested whether spinobulbar lamina I cells respond to muscle contraction. Spinobulbar lamina I neurons were identified in chloralose-anesthetized cats by antidromic activation from the ipsilateral caudal ventrolateral medulla. Static contractions of the ipsilateral triceps surae muscle were evoked by tibial nerve stimulation using parameters that avoid afferent activation, and arterial blood pressure responses were recorded. Recordings were maintained from 13 of 17 L(7) lamina I spinobulbar neurons during static muscle contraction, and 5 of these neurons were excited. Three were selectively activated only by muscle afferents and did not have a cutaneous receptive field. Spinobulbar lamina I neurons activated by muscle contraction provide an ascending link for the reflex cardiorespiratory adjustments that accompany muscular work. This study provides an important first step in elucidating an ascending afferent pathway for somato-autonomic reflexes.

Animals↗
PubMed1990

[Ca2+], not diacylglycerol, is the primary regulator of sustained swine arterial smooth muscle contraction.

Sustained smooth muscle contraction has been proposed to be regulated by either 1) sustained increases in intracellular Ca2+ concentration [(Ca2+]i)-dependent myosin phosphorylation or 2) diacylglycerol-dependent protein kinase C activation. We measured diacylglycerol mass with the diacylglycerol kinase assay and myoplasmic [Ca2+] with aequorin in swine carotid medial smooth muscle. Sustained and significant increases in [Ca2+], myosin light chain phosphorylation, and isometric stress were observed with histamine or endothelin stimulation. Neither stimuli, however, induced significant increases in diacylglycerol mass. Relaxation of histamine-stimulated tissues was induced by removal of histamine or removal of extracellular CaCl2 in the continued presence of histamine. The rate of decline of both [Ca2+] and force was similar in both protocols, suggesting that removal of Ca2+ (without removing the stimulus) was equivalent to removal of the stimulus. These data suggest that [Ca2+]i is the primary regulator of sustained swine arterial smooth muscle contraction, whereas diacylglycerol has, at most, only a minor role.

Alkaloids↗
PubMed2003

Shoulder muscle reflex latencies under various levels of muscle contraction.

Previous research in relaxed muscles shows that muscle reflex latencies are too slow to protect the shoulder. However, during athletic activity when injury occurs, some level of shoulder muscle contraction typically exists. The purpose of the current study was to assess shoulder muscle reflex latencies under various levels of muscle contraction. Seventeen healthy subjects participated. A perturbation consisting of an external rotation collision force to the anterior forearm in a position of apprehension under various levels of muscle contraction (0%, 20%, and 50% of a maximum voluntary muscle contraction) was applied. Muscle reflex latencies were measured as the time from perturbation application to onset of muscle activity. Electromyography measured activity onset of the rotator cuff muscles and the primary humeral movers. During 0%, the latissimus dorsi muscle reflex latency was significantly slower than most other muscles. No difference existed between muscles in the 20% and 50% conditions. For the rotator cuff muscles, the reflex latencies significantly quickened for 20% and 50% compared with the relaxed state (0%). Overall, introducing muscle contraction significantly quickened muscle reflex latencies. These results provide clinicians with a better understanding of the role that these reflexes play in joint stability in a position of injury vulnerability like a position of apprehension.

Adult↗
PubMed2002

Heart rate at the onset of muscle contraction and during passive muscle stretch in humans: a role for mechanoreceptors.

Previous evidence suggests that the heart rate (HR) increase observed with isometric exercise is dependent on different afferent mechanisms to those eliciting the increase in blood pressure (BP). Central command and muscle metaboreceptors have been shown to contribute to this differential effect. However, in experimental animals passive stretch of the hindlimb increases HR suggesting that small fibre mechanoreceptors could also have a role. This has not been previously shown in humans and was investigated in this study. Healthy human volunteers were instrumented to record BP, ECG, respiration, EMG of rectus femoris and gastrocnemius and contraction force of triceps surae. Voluntary isometric contraction of triceps surae elicited a significant HR change in the first three respiratory cycles at 40 % of maximum voluntary contraction whereas BP did not change significantly until after 30 s. This suggests that different mechanisms are involved in the initiation of the cardiovascular changes. Sustained passive stretch of triceps surae for 1 min, by dorsiflexion of the foot, caused a significant (P < 0.05) increase in HR (5 +/- 2.6 beats min(-1)) with no significant change in BP. A time domain measure of cardiac vagal activity was reduced significantly during passive stretch from 69.7 +/- 12.9 to 49.6 +/- 8.9 ms. Rapid rhythmic passive stretch (0.5 Hz for 1 min) was without significant effect suggesting that large muscle proprioreceptors are not involved. We conclude that in man small fibre muscle mechanoreceptors responding to stretch, inhibit cardiac vagal activity and thus increase HR. These afferents could contribute to the initial cardiac acceleration in response to muscle contraction.

Adult↗
PubMedDate not supplied

[Cellular mechanism of muscle contraction of bronchial smooth muscle].

Airway smooth muscle is one of the main effector of bronchial reactivity. The understanding of the cellular mechanisms involved in the contraction of this muscle has advanced in the recent past since isolated cells in culture can now be studied. Extracellular messengers (neurotransmitters and mediators) as well as their specific membrane receptors have been analyzed in some details. The membrane transduction of extracellular messengers brings about the formation (or the increase in the concentration) of the intracellular second messenger which, in airway smooth muscle, is the cytosolic calcium (Ca2+i) via activation of calcium channels which depend on surface membrane potential changes (electromechanical coupling) on the one hand and mainly via mechanisms independent of surface membrane potential changes-so-called the pharmacomechanical coupling--which involves membrane phosphoinositides metabolism. Changes in Ca2+i activate contractile proteins leading the muscle to shorten and to develop force via several controlled steps such as phosphorylation of myosin or changes in the sensitivity to Ca2+ of the contractile elements. Experimental techniques that enable to simultaneously study different aspects of the cellular response are being developed in airway smooth muscle and are likely to provide complementary information about the cellular physiology and pathophysiology of this muscle.

Animals↗
PubMed2002

Smooth muscle contraction by small GTPase Rho.

Abnormal contraction of vascular smooth muscle contributes to a variety of diseases such as hypertension and vasospasm in coronary and cerebral arteries. An increment in a cytoplasmic Ca2+ concentration is the key event in smooth muscle contraction. However, smooth muscle contraction is modified upon the stimulation by agonists as well as in some pathophysiological situations in Ca(2+)-independent mechanism. The molecular mechanism underlying this modulation was not elucidated. Recent studies have shown the important role of small GTPase Rho and its effector, Rho-associated kinase (Rho-kinase)/ROK/ROCK in Ca(2+)-independent regulation of smooth muscle contraction. The Rho/Rho-kinase pathway modulates the phosphorylation level of myosin light chain (MLC) of myosin II, mainly through the inhibition of myosin phosphatase, and contributes to the agonist-induced Ca(2+)-sensitization in smooth muscle contraction. The Rho/Rho-kinase pathway is involved in the pathogenesis of hypertension, vasospasm and arteriosclerosis, and is a potent target of new therapies for these diseases.

Animals↗
PubMed1985

[Dynamics of efferent regulation of muscle contraction. Determination of transition processes: external load--muscle length].

Transition processes of the length changes were studied in the ankle extensors of anesthetized cats in case of abrupt transition from isometric to isotonic condition of muscle contraction which was evoked by distributed stimulation of efferents supplied these muscles. Dynamic properties of muscles were analyzed in the framework of the two-components (inertialess and aperiodic) approximation of the transition processes. These properties were nonlinear because of the complex dependence of time constants and weight of an aperiodic component on the amplitudes of input signals. Both of these parameters were significantly lower in the shortening processes comparing with the lengthening ones. When amplitudes of length changes were small, the average limit values of the time constants were 1.38s for slow soleus muscle shortening and 0.39s for its lengthening. The same parameters for fast muscles (gastrocnemius and plantaris) were 0.55 and 0.25s, respectively. The observed dynamical properties of muscle contraction are discussed for their functional significance.

Animals↗
PubMed2000

Effect of blood flow and muscle contraction on noradrenaline spillover in the canine gracilis muscle.

Many authors have reported that, during exercise, noradrenaline spillover increases and fractional extraction decreases. It has been suggested that the increase in blood flow to active muscles may contribute to these effects. Muscle contraction also causes changes in many factors that may affect noradrenaline spillover and fractional extraction. In this experiment, we studied the effect of muscle contraction and blood flow on noradrenaline and adrenaline spillover and fractional extraction in the in situ canine gracilis muscle. The low intensity stimulation protocol enabled us to have muscle contractions without any effect on the local concentration of noradrenaline, as measured by microdialysis, and noradrenaline spillover. Fractional extraction of both noradrenaline and adrenaline was unaffected by increasing blood flow three and four times its resting value. In addition, noradrenaline spillover was increased by the higher blood flow, from 188 to 452 pg x min(-1) at rest and from 246 to 880 pg x min(-1) during stimulation. Stimulation of muscle contraction caused a significant increase in fractional extraction of noradrenaline and a nonsignificant increase in adrenaline extraction. In addition, an adrenaline spillover was observed in certain conditions. In light of our results, it seems that blood flow may not be the main factor decreasing fractional extraction of noradrenaline during exercise. However, blood flow could contribute to the increase in noradrenaline spillover observed in the active muscles during exercise.

Animals↗