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PubMed1992

The biophysics and biochemistry of smooth muscle contraction.

In this review the biophysics and biochemistry of smooth muscle contraction are dealt with. We describe a new model for the study of bronchial smooth muscle, which facilitates study of cellular contractile mechanisms. A new concept emerging is that study of steady-state mechanical parameters such as maximal isometric force (Po) velocity is inadequate because two types of crossbridges (normally cycling (NBR) and latch) seem to be sequentially active during smooth muscle contraction. Thus quick-release techniques are required to characterize the force-velocity properties of the two types of bridges. Pathophysiological processes that affect the muscle's shortening ability seem to affect the early NBRs only. With respect to maximal shortening capacity of the smooth muscle, the role of loading is very important. The differences between isotonic, elastic, and viscous loading are considerable. Ultimately, the time course and magnitude of loading should exactly resemble that operative in vivo. Once again, it is the characteristic of loading in the early phase of contraction that is crucial, as most of the shortening in smooth muscle occurs early in the contraction. While the maximum force developed by smooth muscle per unit cross-sectional area is the same as for striated muscle, the velocity is 50 times less. The properties of the series and parallel elastic elements of smooth muscle are described. The latter, when in compression mode, acts as an internal resistance to shortening and probably limits it. Isotonic relaxation has therefore not been studied in smooth muscle. We have developed a shortening parameter that is independent of the load on the muscle and of the initial length of the muscle's contractile element. We report the novel observation that isotonically relaxing smooth muscle reactivates itself, resulting in terminal slowing of the relaxation process. With respect to the biochemistry of smooth muscle contraction, contractile (actin isoforms, myosin heavy and light chains and their isoforms), regulatory (calmodulin-4 Ca2+, myosin light chain kinase, myosin light chain and its phosphorylation, tropomyosin, caldesmon, and calponin), and cytoskeletal (chiefly desmin and vimentin) proteins are discussed. While the kinase activates the contractile system, caldesmon and calponin modulate the activity downward. The cytoskeletal proteins desmin, vimentin, and alpha-actinin could constitute the muscle cell's internal resistor.

Animals↗
PubMed2004

The role of the vagus nerve in hypertonic resuscitation of hemorrhagic shocked dogs.

Previous studies have suggested a critical role for the vagi during the hypertonic resuscitation of hemorrhagic shocked dogs. Vagal blockade prevented the full hemodynamic and metabolic recovery and increased mortality. This interpretation, however, was challenged on the grounds that the blockade also abolished critical compensatory mechanisms and therefore the animals would die regardless of treatment. To test this hypothesis, 29 dogs were bled (46.0 +/- 6.2 ml/kg, enough to reduce the mean arterial pressure to 40 mmHg) and held hypotensive for 45 min. After 40 min, vagal activity was blocked in a reversible manner (0 masculine C/15 min) and animals were resuscitated with 7.5% NaCl (4 ml/kg), 0.9% NaCl (32 ml/kg), or the total volume of shed blood. In the vagal blocked isotonic saline group, 9 of 9 dogs, and in the vagal blocked replaced blood group, 11 of 11 dogs survived, with full hemodynamic and metabolic recovery. However, in the hypertonic vagal blocked group, 8 of 9 dogs died within 96 h. Survival of shocked dogs which received hypertonic saline solution was dependent on vagal integrity, while animals which received isotonic solution or blood did not need this neural component. Therefore, we conclude that hypertonic resuscitation is dependent on a neural component and not only on the transient plasma volume expansion or direct effects of hyperosmolarity on vascular reactivity or changes in myocardial contraction observed immediately after the beginning of infusion.

Animals↗
PubMed1975

Ureterometrographic studies on human subjects with normal urinary tract system.

Ureteral motility was studied in 40 subjects with normal urinary tract systems. Although the contraction waves were often monophasic in shape some were characterised by the presence of a notch on the contraction or relaxation limb of the peristaltic complex, indicating that notched complexes do not necessarily signify obstructive uropathy. Retrograde filling of the bladder to within its physiologic limits with isotonic saline solution markedly changed the pattern of the ureteral activity.

Adolescent↗
PubMed1991

[Contractile responsiveness of the isolated guinea pig oviduct to autacoids at different phases of the sexual cycle or under ovarian steroid treatment].

Contraction of the longitudinal smooth muscle of the isolated guinea pig oviduct in response to autacoids was examined at different phases of the sex cycle or during ovarian steroid treatments. Isolated strips from isthmic smooth muscle of the female guinea pig (body weight; 300-900 g) oviduct were mounted in an organ bath and their isotonic responses were measured in the longitudinal direction. Histamine (greater than or equal to 3 X 10(-8) M) produced a concentration-dependent contraction of the oviductal smooth muscle, which was unaffected by the sex cycle. Noradrenaline and adrenaline (greater than or equal to 10(-8) M) produced a contraction mediated by alpha-adrenoceptors and a relaxation mediated by beta-adrenoceptor. During proestrus and metestrus (high estrogen), the contractile response was reduced but relaxation was increased, compared with those observed during diestrus. Prostaglandin E2 and F2 alpha (greater than or equal to 10(-10)M and greater than or equal to 10(-9)M, respectively) produced a concentration-dependent contraction and their maximum responses were about 50% of that induced by histamine (10(-4)M). These contractile responses were unaffected by the sex cycle. On the other hand, acetylcholine did not modify the smooth muscle tone of the isolated guinea pig oviduct in the concentration range from 10(-7)M to 3 X 10(-4)M. The contractile response of the oviductal smooth muscle to adrenaline after bilateral ovariectomy was inhibited by estrogen treatment, while relaxation was inhibited by progesterone treatment.

Animals↗
PubMed1988

Irreversible injury of isolated adult rat myocytes. Osmotic fragility during metabolic inhibition.

Isolated myocytes can be established as a valid model for studying changes in cytoskeletal proteins during the development of irreversible injury only if isolated cells develop lesions similar to those that occur during irreversible injury to intact hearts, specifically osmotic fragility and subsarcolemmal blebs. In the first experiment, isolated cells were irreversibly injured by metabolic inhibition with 5 mM Iodoacetic acid (IAA) and 6 mM amobarbital (Amy). Osmotic fragility of control and injured cells was determined by comparing the rates of development of trypan blue permeability during 60 minutes of isotonic or hypotonic (50% reduction in osmolality) incubations. Cell morphology was monitored by light and electron microscopy. Control cells remained elongated and excluded trypan blue. Metabolically inhibited cells rapidly contracted to a nearly square shape. The inhibited squared cells initially excluded trypan blue, but during 60 minutes of incubation became permeable to trypan blue. Cells in hypotonic buffer developed blue staining at a more rapid rate than cells in isotonic buffer, indicating increased osmotic fragility. In a second experiment, control and inhibited cells were first incubated for 25 minutes in isotonic buffer and then in either isotonic or hypotonic buffer. In this experiment, inhibited cells also developed more extensive and rapid permeability increases when transferred to the hypotonic buffer than cells maintained in the isotonic buffer. In both experiments, increased permeability of cells to trypan blue was accompanied by formation of subsarcolemmal blebs along the lateral cell border and at the intercalated disks. The results show that metabolically inhibited, isolated myocytes do exhibit morphologic lesions and increased osmotic fragility properties similar to those reported during anoxic or ischemic injury to intact hearts. Therefore, isolated myocytes may be a useful model with which to study cytoskeletal-sarcolemmal membrane changes during development of irreversible injury.

Animals↗
PubMed1994

Vagal reflex inhibition of motility in the abomasal body of sheep by antral and duodenal tension receptors.

Vagally-mediated regulation of motility in the abomasal body by duodenal and abomasal antral motility was demonstrated in acutely prepared anaesthetized sheep. The enteric plexuses between the abomasal body, antrum and duodenum were interrupted by transection. Antral contractions were more effective than duodenal contractions at causing inhibition of the abomasal body, and antral isometric conditions were more effective than antral isotonic conditions. Inhibition of motility in the abomasal body was reduced by unilateral cervical vagotomy, was abolished by bilateral cervical vagotomy, and was reversibly inhibited by cervical vagus cold block. The demonstration of vagal pathways in abomaso-abomasal reflexes confirms a functional homology of the mechanisms in the ruminant and animals with simple forms of stomach.

Abomasum↗
PubMed1991

Effects of 8-bromo-cyclic GMP on contraction and on inotropic response of ferret cardiac muscle.

The effects of guanosine 3':5'-cyclic monophosphate (cGMP) on cardiac contraction are not established. Using isolated electrically-stimulated ferret papillary muscle at 29 degrees C, 2.0 mM calcium we investigated the effects of 8-Bromo-cGMP on (a) basal contraction for comparison with the effects of reduction in extracellular calcium or of reduction in resting muscle length; (b) contraction of preparations stimulated by isoprenaline, the dihydropyridine calcium agonist Bay K8644 or post-extrasystolic potentiation. 8-Bromo-cGMP (0.1 mM) induced a small significant reduction in isometric twitch tension (TT) (7%), isotonic shortening (PS) (6%) and in twitch duration, but had no effect on maximum unloaded shortening velocity (Vmax) or rate of tension development (+dT/dt). Reduction in muscle length induced a similar immediate effect on contraction. Reduction of extracellular calcium (2.0 mM to 1.25 mM) reduced TT by 24% and PS by 14% as well as Vmax (19%) and +dT/dt (29%), but did not alter twitch duration. Bay K8644 (0.01 to 10 microM) produced increases in TT, +dT/dt, PS and twitch duration each of which was significantly reduced in the presence of 8-Bromo-cGMP (0.1 mM). 8-Bromo-cGMP had no effect on the responses to isoprenaline 1 nM to 100 microM--which increased TT, +dT/dt and PS but markedly reduced twitch duration--nor on post-extrasystolic potentiation which increased TT and +dT/dt but slightly reduced twitch duration. These results show that 8-Bromo-cGMP induces changes similar to the immediate effects of reduction in resting muscle length, and reduces the positive inotropic effects of Bay K8644 but not those of isoprenaline or post-extrasystolic potentiation.

3-Pyridinecarboxylic acid, 1,4-dihydro-2,6-dimethy↗
PubMedDate not supplied

Contractile response to neuropeptide Y of rat isolated duodenum.

The response of isolated duodenum to neuropeptide Y (NPY) was studied isotonically in neonatal and adult rats. Neuropeptide Y (10(-8) to 10(-6) M) elicited a biphasic contraction of isolated duodenum from neonatal rats, but monophasic and weak contraction of adult duodenum. The first phase of NPY-induced contraction of neonatal duodenum was concentration dependent and partially inhibited by preincubation with tetrodotoxin, a Na+ channel blocker, hyoscine, a muscarinic antagonist, suramin, a P2 purinoceptor antagonist, and indomethacin, an inhibitor for prostaglandin biosynthesis. Neuropeptide Y(13-36), a specific Y2 NPY receptor agonist, elicited a concentration-dependent contraction of neonatal rat duodenum. The duodenal response to NPY thus changes during development in rats. Both cholinergic and purinergic transmission and prostaglandin biosynthesis may be involved in the NPY-induced contraction of neonatal duodenum. Neuropeptide Y-induced contraction may be mediated through presynaptic Y2 receptors.

Animals↗
PubMed1990

Dissociation between myosin phosphorylation and shortening velocity in canine trachea.

The relationship between glycogen phosphorylase activity (an index of cytosolic Ca2+ content), myosin light-chain phosphorylation, isotonic shortening velocity, and isometric tension was examined in canine trachealis. Responses were measured in tracheal strips contracted with various concentrations of methacholine or K+. Both agonists produced prolonged and concentration-dependent increases in isometric tension that reached 90% of the plateau level within 1 (methacholine) to 5 (K+) min and remained stable over 60 min. In contrast to the monotonic increase in isometric tension, shortening velocity reached a maximum almost immediately (12-48 s) after the addition of either methacholine or K+ and then declined over time to a steady-state level that was 25-40% of the peak. Phosphorylase activity also increased transiently, reaching a maximum 1-2 min after the addition of either agonist before declining to near-basal levels over the 60-min observation period. Unlike the increases in shortening velocity and phosphorylase activity, agonist-induced myosin phosphorylation was not markedly transient. Moreover, regardless of the contractile agonist used, no correlation was found between myosin phosphorylation and shortening velocity when these parameters were compared at corresponding time points. This suggests that myosin phosphorylation is not the sole determinant of shortening velocity in canine trachealis.

Animals↗
PubMed1983

Airway smooth muscle mechanics: reduced activation and relaxation.

Reduced activation of skeletal muscle fibers at below-optimal lengths has been reported before. We studied tracheal smooth muscle (TSM) as a model of airway smooth muscle to see whether such a phenomenon existed in smooth muscle also; we found that active length-tension curves at normal and raised Ca2+ concentrations were significantly different. This indicated reduced activation of the TSM at below-optimal lengths. This reduction was in addition to that arising from the length-tension effect. We also studied the mechanics of relaxation in TSM and noted that in afterloaded isotonic tension records the time course of TSM relaxation appeared to closely follow that of the isometric contraction at all loads. In this it differed markedly from relaxation in skeletal muscle where the time courses of relaxation at different loads differed from each other and from that of the isometric muscle.

Animals↗
PubMed2000

Vascular smooth muscle mechanics in isolated perfused segments of carotid arteries.

BACKGROUND: We hypothesized that smooth muscle contraction and relaxation responses in a muscle bath (isometric tension) would be different than responses of intact vessels (isotonic tension). METHODS: Bovine carotid artery contractile responses to the catecholamine, norepinephrine, and smooth muscle relaxant, 3-isobutyl-1-methylxanthine, were examined in strips of vessels in a muscle bath and in intact whole vessels in an isolated perfused whole-vessel perfusion apparatus. RESULTS: The maximal tension in the muscle bath depended on the length of the strip. The responses of whole vessels to increasing pressure was curvilinear. The maximal decrease in vessel diameter in intact vessels in response to the catecholamine and norepinephrine occurred at low intraluminal pressures. The dose-response curve to norepinephrine was shifted to the left in intact vessels compared with strips of vessels in the muscle bath, which suggests that whole vessels were more sensitive to norepinephrine. The maximal increase in diameter to increasing intraluminal pressure occurred in the presence of the phosphodiesterase inhibitor, 3-isobutyl-1-methylxanthine, which suggests that there was significant intrinsic tone in the vascular smooth muscle. CONCLUSIONS: These results suggest that there are differences in the contractile properties of the vascular smooth muscle that are related to the ex vivo system used to examine smooth muscle responses. Responses obtained in isolated perfused whole vessels may more closely approximate in vivo responses.

1-Methyl-3-isobutylxanthine↗
PubMed1982

Direct measurement of sarcomere length from isolated cardiac cells.

Isolated cardiac muscle cells enzymatically digested with collagenase and hyaluronidase from whole rat myocardium demonstrate the characteristics of an intact membrane in that they tolerate millimolar concentrations of free Ca2+ and exhibit phasic contractions with electrical excitation. These isolated cells maintain their characteristic A-I band striation patterns when at rest or during contraction. An apparatus has been developed to directly image these cells with phase-contrast micrography onto a 1,728-element charge-coupled device photodiode array for rapid data storage in a digital computer. The digitized striation pattern profile was analyzed for individual and average sarcomere spacing. In isotonic media the average resting sarcomere length ranged from 1.77 to 1.91 micrometers in 13 cells, with a mean length of 1.83 +/- 0.12 micrometers. Electrically stimulated phasic contractions in three cells demonstrated a synchronous 20% decrease in sarcomere spacing to a mean of 1.51 micrometers. Striation spacing decreased under hypertonic stress but elongated only up to 1.93 micrometers in hypotonic solutions, suggesting that some internal elastic constraint exists that limits elongation of the cell.

Animals↗
PubMed1976

A mechanochemical model for the steady and transient contractions of the skeletal muscle.

A mechanochemical model for muscle contraction was presented which consisted of three subsystems: the regulatory mechanism of contraction by Ca ion, the cross-bridge cycle coupled with actin-myosin interaction and the dynamics of contraction with an external load. It was assumed that both the rate constant of the cross-bridge cycle and the net force of the cross-bridge were linear functions of the sliding velocity. Most parameters in the model were determined from the experimental data, but several were estimated by simulation techniques. The model adequately described the force-load-velocity relation, the rates of energy and heat output as well as some basic mechanical properties of muscle. Not only the steady-state contraction but also the twitch response could be explained by the model. Time courses of tension and shortening during isometric and isotonic twitches were calculated by the model on a digital computer. The calculated curves agreed satisfactorily with the experimental ones obtained from the frog semitendinosus muscle. The rate of tension rise of the isometric twitch was shown to attain the peak at nearly the same time as does the calculated Ca concentration curve.

Actins↗
PubMed1992

Endothelin increases myofilament Ca2+ sensitivity in alpha-toxin-permeabilized rabbit mesenteric artery.

This study was designed to investigate the mechanism of endothelin-1 (ET-1) contractions in Staphylococcus alpha-toxin-permeabilized vascular smooth muscle. Rabbit small mesenteric arteries permeabilized with alpha-toxin were mounted for isometric or isotonic force recording or were processed for determination of myosin light chain (MLC) phosphorylation levels. Addition of 100 nM ET-1 plus 10 microM GTP significantly enhanced myofilament Ca2+ sensitivity as compared with the addition of Ca2+ alone (EC50, 0.47 microM Ca2+ for Ca2+ alone and 0.13 microM Ca2+ for ET-1 plus (GTP). This enhanced sensitivity was reversed by GDP beta S. ET-1-induced contractions were relaxed at a constant [Ca2+] by the addition of 30 microM cAMP or cGMP, demonstrating a direct effect of the cyclic nucleotides on contractile regulation. Inhibition of protein kinase C activity by 100 nM staurosporine relaxed ET-1 plus GTP-induced contractions, and pretreatment with 40 microM chelerythrine inhibited the ET-1 plus GTP increase in force. At 0.32 microM Ca2+, steady-state levels of shortening velocity were not increased by ET-1 plus GTP, although steady-state levels of MLC phosphorylation were significantly enhanced. The ET-1-induced increase in MLC phosphorylation was not altered by changes in [Ca2+], whereas the shortening velocity was Ca2+ dependent, suggesting that the increase MLC phosphorylation level may be the result of protein kinase C, rather than MLC kinase, activation. These results are consistent with the hypothesis that ET-1 increases myofilament Ca2+ sensitivity by a G protein-dependent pathway and subsequent activation of protein kinase C.(ABSTRACT TRUNCATED AT 250 WORDS)

Actin Cytoskeleton↗
PubMed2006

Hyperkalemic cardioplegia-induced myocyte swelling and contractile dysfunction: prevention by diazoxide.

BACKGROUND: Hyperkalemic cardioplegia (9 degrees C) results in significant myocyte swelling and reduced contractility, representing a possible mechanism of myocardial stunning. Adenosine triphosphate-sensitive potassium channel (KATP) openers have been shown to ameliorate stunning. This study evaluated the hypothesis that a KATP opener would prevent hyperkalemic cardioplegia-induced myocyte swelling and reduced contractility. METHODS: Isolated rabbit myocytes were perfused with 37 degrees C Tyrode's solution for 20 minutes, followed by test solution (9 degrees C or 37 degrees C) including control Tyrode's, Tyrode's + 100 micromol/L diazoxide (KATP opener), St. Thomas's solution; or 9 degrees C St. Thomas's + 100 micromol/L diazoxide or St. Thomas's + 100 micromol/L diazoxide + 20 micromol/L HMR1098 or 50 micromol/L 5-hydroxydeconoate (KATP blockers) for 20 minutes (n = 8 per group). Myocytes were then reexposed to 37 degrees C Tyrode's solution for 20 minutes. Volume and contractility were measured by videomicroscopy and video-based edge detection, respectively. RESULTS: St. Thomas's solution (9 degrees C) caused significant myocyte swelling and associated reduced contractility (p < 0.05). The addition of diazoxide abolished myocyte swelling (p < 0.0001), and eliminated the associated reduced contractility (p < 0.05). Findings were unchanged by the addition of HMR 1098 and 5-hydroxydeconoate. CONCLUSIONS: Diazoxide prevented myocyte swelling and reduced contractility secondary to hyperkalemic cardioplegia, and this was unchanged by the addition of either KATP channel blocker. Prevention of myocyte swelling was associated with improved contractility, consistent with the hypothesis that myocyte swelling may be a mechanism of myocardial stunning. Diazoxide may play a role in myocyte volume homeostasis by means of a mechanism separate from opening the KATP channel.

Animals↗
PubMed1993

The effect of serotonin on the rabbit isolated iris sphincter muscle.

The rabbit isolated iris sphincter muscle maintained in an isotonic state is unaffected by applied serotonin (5-hydroxytryptamine or 5-HT) whereas carbachol causes the muscle to contract. Serotonin does, however, produce a relaxation of the contracted muscle in a dose-dependent manner. This effect is also induced by the 5-HT receptor agonists 8-OH-DPAT (8-hydroxy-2-[di-n-propyl-amino] tetralin, RU 24969 (5-methoxy-3-[1,2,3,6, tetrahydro-4-pyridinyl]-1-indole) and ipsapirone, suggesting the involvement of 5-HT1A receptors. This view is supported by the finding that metergoline, methysergide and propranolol all counteracted the effect produced by serotonin. While 5-HT3 receptors are not involved in the described process, a minor involvement of 5-HT2 receptors cannot be excluded as methysergide partially counteracted the serotonin response. These data provide evidence that serotonin receptors, in particular the 5-HT1A subtype, may be associated with the iris sphincter muscle and suggest their involvement in the regulation of pupil size.

Animals↗