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PubMed2000

Kinetic equilibrium of forces and molecular events in muscle contraction.

In biomolecular systems, the mechanical transfer of free energy occurs with both high efficiency and high speed. It is shown here that such a transfer can be achieved only if the participating free-energy-storing elements exhibit opposing relationships between their content of free energy and the force they exert in the transfer direction. A kinetic equilibrium of forces (KEF) results, in which the transfer of free energy is mediated essentially by thermal molecular motion. On the basis of present evidence, KEF is used as a guiding principle in developing a mechanical model of the crossbridge cycle in muscle contraction. The model allows the basic features of molecular events to be visualized in terms of plausible structures. Real understanding of the process will require identification of the elements that perform the functions described here. Besides chemomechanical energy transduction, KEF may have a role in other biomolecular processes in which free energy is transferred mechanically over large distances.

Actins↗
PubMed1997

Effects of the non-peptide B2 antagonist FR173657 on kinin-induced smooth muscle contraction and relaxation, vasoconstriction and prostaglandin release.

1. The non-peptide bradykinin (BK) antagonist (E)-3-(6-acetamido-3-pyridyl)-N-[N-[2,4-dichloro-3-[(2-methyl-8-quinolin yl) oxymethyl]phenyl]-N-methylaminocarbonylmethyl]acrylamide (FR173657) was tested in intestinal, uterine, tracheal and vascular in vitro preparations. The investigation aimed at determining the antagonistic potency, duration of action, specificity for BK receptors and apparent mode of antagonistic action of FR173657. 2. Contractions of the isolated ileum of the guinea-pig in response to BK were inhibited by FR173657 (10-300 nM) in a concentration-dependent manner. The inhibition lasted for up to 90 min after wash-out of FR173657. Cumulative concentration-response curves to BK were shifted to the right with a concomitant decrease in the maximum effect. A pKB value of 8.7 was determined. FR173657 had no effect on contractions induced by acetylcholine, histamine, 5-hydroxytryptamine, substance P, angiotensin II or caerulein. 3. The concentration-response curves for B2 receptor-mediated relaxations of the rat isolated duodenum induced by BK were shifted to the right together with a concomitant reduction of the maximum BK effect in the presence of FR173657 (10-300 nM). A pKB of 9.0 +/- 0.2 was calculated. FR173657 had no effect on B1 receptor-mediated relaxations in response to des-Arg9-BK. 4. The concentration-response curves for BK-induced contractions of the rat isolated uterus were shifted to the right by FR173657 (3-300 nM) in a concentration-dependent and parallel manner. The Schild plot for the inhibition caused by FR173657 had a slope of -0.98 indicating a competitive mode of antagonism. A pA2 value of 9.1 was determined. 5. Contractions of the circular smooth muscles of the guinea-pig isolated trachea in response to BK were concentration-dependently inhibited by FR173657 (10-100 nM). An affinity estimate of 9.3 was calculated for FR173657. Contractions induced by acetylcholine and relaxations in response to isoprenaline remained completely unaffected by FR173657. 6. In the rabbit isolated perfused ear, BK (0.01-10 nmol) produced a dose-dependent vasoconstriction. In the presence of 30 nM FR173657, the effects of BK were reduced by at least 60%, while FR173657 completely abolished the effects of all BK doses at 300 nM. FR173657 did not affect vasoconstriction induced by noradrenaline or angiotensin II. 7. The arterial injection of BK (10 nmol) into the rabbit isolated perfused ear caused an approximately three fold increase in the release of the prostaglandins E2 and I2 into the venous effluent. The BK-stimulated prostaglandin release was completely abolished in the presence of FR173657 (300 nM) while the basal prostaglandin release was unchanged. 8. In summary, FR173657 was shown to be a highly potent and selective BK antagonist which was active on B2, but not B1, receptors. FR173657 was a competitive antagonist in the rat uterus but showed a deviation from competitive inhibition in the other preparations studied similar to other second generation peptide antagonists. The inhibitory action in vitro was long-lasting, but was fully reversible.

Animals↗
PubMed2001

Antidiarrheal activity of wood creosote: inhibition of muscle contraction and enterotoxin-induced fluid secretion in rabbit small intestine.

Wood creosote has long been used as an antidiarrheal agent, but its mechanism of action is not well understood. To elucidate the mechanism of its antidiarrheal activity, we have addressed questions whether it inhibits fluid secretion induced by Escherichia coli heat-stable enterotoxin (STa) in rabbit jejunum in vivo, and whether it inhibits muscle contraction of isolated rabbit ileum ex vivo. Wood creosote (10-100 mg/l) instilled in a ligated loop of jejunum inhibited STa-induced fluid secretion (p < 0.05). It also inhibited the spontaneous phasic, acetylcholine-induced tonic and Ba2+-induced tonic contractions of longitudinal and circular muscles of ileum dose-dependently with IC(50) values of 130-530 mg/l. These data provide further evidence that the antidiarrheal activity of wood creosote is attributable to its antisecretory and antimotility effects.

Acetylcholine↗
PubMed1989

Reproducible stimulation of ciliary muscle contraction in the cynomolgus monkey via a permanent indwelling midbrain electrode.

To better study the pivotal role of the ciliary muscle in ocular accommodation and aqueous humor outflow, a technique was developed to permit long-term reproducible stimulation of the muscle via the normal efferent neuronal pathway in cynomolgus monkeys. Following a small midline craniotomy, the stereotaxic coordinates of the Edinger-Westphal (E-W) nucleus were localized by contrast ventriculoradiography. A bipolar stimulating electrode was stereotaxically positioned to generate the maximum accommodative amplitude, and then permanently affixed to the surrounding cranium. Once experience was gained, the implant procedure required approximately 3 h and was well-tolerated by the animals, which subsequently exhibited normal behavior and no apparent discomfort or neurological deficits. Most animals retained the implant seemingly permanently (8-42 months follow-up), although a few animals extruded them after 4-8 months. Electrode placement in the E-W nucleus was verified histologically. The stimulation current and frequency-accommodative response relationships varied remarkably little between eyes, animals, or experimental sessions, although there was moderate inter-animal variation in the maximum accommodative amplitude. Using square-wave pulses of 0.5 ms duration, maximum accommodation, averaging approximately 15 diopters, was achieved at approximately 700 microA and approximately 70 Hz, and was greater under pentobarbital than under halothane anesthesia. Topical application of carbachol, eserine and echothiophate to the eye induced more accommodation than did central electrical stimulation. Permanent implantation of a stimulating electrode into the E-W nucleus may facilitate study of ocular physiological parameters dependent upon ciliary muscle contraction.

Accommodation, Ocular↗
PubMed1986

Activation of smooth muscle contraction: relation between myosin phosphorylation and stiffness.

Contraction and myosin light-chain phosphorylation were measured in electrically stimulated tracheal smooth muscle. Latencies for the onset of force, stiffness, and light-chain phosphorylation were 500 milliseconds. Myosin light chain was phosphorylated from 0.04 to 0.80 mole of phosphate per mole of light chain with a pseudo-first-order rate of 1.1 per second with no evidence of an ordered or negatively cooperative process. Following the period of latency, stiffness increased with phosphorylation and both increased more rapidly than isometric force. The linear relation between stiffness and phosphorylation during activation suggests independent attachment of each myosin head upon phosphorylation.

Animals↗
PubMed1983

Enhancement and prolongation of vascular smooth muscle contraction by aldosterone.

Isolated rings of rabbit thoracic aorta were mounted in tissue baths for the measurement of isometric tension development and desipramine was added to all baths to block neuronal uptake of catecholamines. When these vessels were contracted to a steady-state of 1.5-3.5 g with norepinephrine, the addition of 1, 10 and 100 microM aldosterone caused a further contraction of 0.09, 0.47 and 0.8 g, respectively. Vessels contracted with norepinephrine and exposed to aldosterone were also immersed in mineral oil to trap a finite amount of norepinephrine within the receptor compartment of the tissue and the rate of relaxation was measured. The time to relax 50% (t1/2) in the presence of 100 microM aldosterone was approximately 18 min, while that in the presence of either ethanol diluent or 10 microM aldosterone was 7 min. When maximally effective concentrations of aldosterone and deoxycorticosterone acetate were used, the increases in norepinephrine-induced contractions and relaxation t1/2 values caused by these agents were identical. Combining these agents did not produce additive effects. Aldosterone also increased contractions and t1/2 values in tissues contracted with epinephrine but not in those contracted with methoxamine or 5-hydroxytryptamine. These findings support the conclusion that aldosterone enhances and prolongs contraction by inhibiting the removal of catecholamines from the receptor compartment of vascular smooth muscle.

Aldosterone↗
PubMed2006

Vasodilation and vascular control in contracting muscle of the aging human.

There is accumulating evidence in humans that the control of blood flow to dynamically contracting skeletal muscle is altered with normal aging. Despite some inconsistencies in the literature, most healthy older subject groups studied to date (approximately 55-75 years) exhibited attenuated leg blood flow responses to moderate intensity leg exercise in comparison to younger (approximately 20-30 years) controls. In most cases, older subjects also have higher arterial perfusion pressures at rest and at any submaximal workload than their younger counterparts, suggesting a heightened level of vasoconstriction in the legs that could result from structural and/or functional alterations within the arterial vasculature. The influence of age on vasodilator responsiveness in the contracting limbs of humans remains an open question, with reports of blunted, similar, and augmented increases in local vascular conductance during graded exercise in older vs. younger adults. Recent results from the authors' laboratory suggest that the ability of vascular smooth muscle in the legs to dilate in response to physiological and pharmacological stimuli is relatively well preserved with advancing age in men; however, a sex difference may exist in that older estrogen-deficient women exhibit blunted leg vasodilator responses compared to younger women. Potential mechanisms underlying altered vascular control within the resistance vasculature of contracting muscles of older men and women remain to be determined, but could include (1) fewer, smaller, and/or stiffer vessels, (2) impaired endothelium-dependent vasodilation, (3) augmented sympathetic vasoconstriction, (4) alterations in metabolic or myogenic control, and (5) reduced effectiveness of the skeletal muscle pump. Systematic research involving both humans and animal models will be necessary to fully elucidate the mechanisms underlying compromised muscle blood flow in old age.

Adult↗
PubMed1984

Changes in intracellular pH and inorganic phosphate concentration during and after muscle contraction as studied by time-resolved 31P-NMR. Alkalinization by contraction.

The changes in intracellular pH and concentration of inorganic phosphate (Pi) were studied during and after contraction of bullfrog sartorius muscles by using 31P-NMR. The intracellular pH was 7.04 in resting muscles at 4 degrees C and an alkalinization by as much as 0.08 pH unit occurred following 5 s tetanic contraction. During the recovery period after contraction the increased level of intracellular pH returned to the resting level, the time course of which coincided with that of the recovery of the Pi concentration. Based on the changes in the intracellular pH and Pi concentration, the buffering power was estimated to be 18 mM/pH unit.

Animals↗
PubMed1988

Regulation of muscle contraction and relaxation in heart.

The calcium uptake and release machinery in heart SR have been characterized: (1) The calcium pump membrane is involved in energized Ca2+ uptake enabling muscle to relax. The calcium pump protein (CPP) in heart SR is modulated by protein kinase phosphorylation of phospholamban lowering the KCa2+. We conclude that in the membrane, phospholamban elevates KCa2+ of calcium pump protein. Phosphorylation of phospholamban attenuates the influence of phospholamban. In the limit, the intrinsic KCa2+ of calcium pump protein in heart and skeletal muscle are approximately the same. (2) The junctional face membrane is involved in calcium release which triggers muscle contraction. Ryanodine is a specific modulator of the Ca2+ release channels of SR which are involved in excitation-contraction coupling. The ryanodine receptor has been isolated, found to be equivalent to the feet structures, and on reconstitution into bilayers, identified as the calcium release channel of SR. The calcium release channel of SR is closed by ruthenium red and Mg2+ and opened by Ca2+ and ATP and low ryanodine concentration. The calcium release channel of SR is not effected by drugs such as nitrendipine, diltiazem and D-600 which modulate the slow inward Ca2+ channel of the plasmalemma/transverse tubule. (3) The calcium release channels from heart and skeletal muscle SR are similar but not identical (Table IV). Important differences distinguish the calcium release machinery in heart from that of skeletal muscle. 1. In heart there are two sources of calcium fluxes: a) extracellular Ca2+ enters via the plasmalemma slow inward calcium current; and b) "Ca2+ induced Ca2+ release" from SR. In skeletal muscle, SR is the single main source of calcium which enters via "Depolarization induced calcium release". 2. The calcium release channel from heart SR has a lower Mr approximately 340,000 vs 360,000 for skeletal muscle. 3. Ryanodine binding in cardiac SR is distinct from that in skeletal muscle (Fig. 7). 4. The isolated calcium release channel from heart SR is more sensitive to Ca2+ for calcium release (Hymel et al. 1988c). Significant progress has been achieved in identifying the calcium release channel of SR in heart and skeletal muscle. The focus of excitation-contraction coupling now shifts to defining the precise nature of the coupling of excitation to contraction.

Animals↗
PubMed1996

Muscle contraction: the step-size distance and the impulse-time per ATP.

We derive the step-size distance, and the impulse time per ATP split, from a consideration of Hill's energy rate equation coupled with the enthalpy available per ATP split. This definition of step-size distance is model-independent, and is calculated to have a maximum of 17 A at no load and to reduce to zero at isometric tension, since it will depend on the velocity of shortening. We revisit a derivation of Hill's force-velocity equation depending on impulsive forces working against frictional forces and show that this gives a physical meaning to Hill's constants a and b. This is particularly elegant for Hill's constant b, which is directly related to the impulse time; the value of this impulse time is 1/2 ms. The question that muscle contraction may involve overlapping interactions is considered. However, we find that the step-size distance is not dependent on the possibility of overlapping interactions.

Actins↗
PubMed1996

Microdialysis of a non-NMDA receptor antagonist into the L7 dorsal horn attenuates the pressor response to static muscle contraction but not passive stretch in cats.

Mean arterial pressure (MAP) and heart rate (HR) were measured during static contraction or passive stretch of the triceps surae muscle of chloralose-anaesthetized cats. MAP and HR increased by 46 +/- 5 mmHg and 17 +/- 3 beats min-1, respectively, during a 1 min contraction. Passive stretch of the same muscle for 1 min reflexly increased MAP and HR by 40 +/- 7 mmHg and 14 +/- 3 beats min-1, respectively. Microdialysis of 2 mM 6-cyano-7-nitroquinoxaline-2,3-dione (CNX), a non-NMDA receptor antagonist, into the dorsal horn at the L7 spinal level attenuated the reflex pressor response to static contraction (2 h of dialysis: delta MAP = 23 +/- 5 mmHg, delta HR = 8 +/- 2 beats min-1). By contrast, there was no attenuation of the pressor response to passive stretch at 2 h of CNQX perfusion. However, the simultaneous microdialysis of 2 mM CNQX into the L6 and S1 levels blunted the pressor and tachycardic responses to contraction and stretch. These data show that the reflex pressor response to static muscle contraction is partly mediated by activation of non-NMDA receptors at the level of afferent fibre entry into the dorsal horn and through collateral pathways. Further, it appears that the afferent pathways within the dorsal horn for the signal transduction arising from static muscle contraction and passive stretch of the hindlimb are dissimilar.

6-Cyano-7-nitroquinoxaline-2,3-dione↗
PubMed1994

Molecular movements in contracting muscle: towards "muscle--the movie".

The recent publication of the crystal structures of G-actin and of myosin subfragment-1, together with analysis of a time-resolved series of well sampled low-angle 2D X-ray diffraction patterns from bony fish muscle permits the study of the molecular movements in muscle that are associated with generation and regulation of contractile force. Here it is shown that even though low-angle (i.e. low resolution) X-ray diffraction patterns are being used, these patterns are sensitive, for example, to sub-domain movements of as little as 3 A or 4 degrees within the actin monomers of actin filaments. Actin filament diffraction patterns from whole muscle are being used to define actin domain and tropomyosin movements involved in regulation. Myosin and actin filament diffraction patterns are being used together to start to show how the complete "quasi-crystalline" unit cell in the bony fish muscle A-band can be modelled as a series of time-slices through a typical tetanic contraction of the muscle. In this way, the time sequence of images can be used to create "muscle--the movie".

Actins↗