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PubMed1995

Bradykinin B1 receptors in the rabbit urinary bladder: induction of responses, smooth muscle contraction, and phosphatidylinositol hydrolysis.

1. The aim of this study was to analyse the pharmacological characteristics, and second-messenger coupling-mechanisms, of bradykinin B1 receptors in an intact tissue, the rabbit urinary bladder; and to investigate the influence of inhibition of endogenous peptidases on kinin activities. 2. In preparations of rabbit mucosa-free urinary bladder, at 90 min after mounting of the preparations, bradykinin (1 nM-10 microM) evoked contractile responses. In contrast, the B1 receptor-selective agonist [des-Arg9]-BK (10 mM-10 microM) was only weakly active at this time. Contractile responses to [des-Arg9]-BK increased with time of tissue incubation in the organ bath, reaching a maximum after 3 h, when the pD2 estimates were 6.4 +/- 0.3 for bradykinin, and 6.9 +/- 0.2 for [des-Arg9]-BK. 3. Once stabilized, responses to [des-Arg9]-BK in the bladder were competitively antagonized by the B1 receptor-selective antagonists [Leu8,des-Arg9]-BK and D-Arg-[Hyp3,Thi5,D-Tic7,Oic8,des-Arg9]-BK ([des-Arg10]-Hoe140) (pKB estimates were 6.1 +/- 0.1 and 7.1 +/- 0.1, respectively; n = 17-21), but responses were unaffected by the B2 receptor-selective antagonist D-Arg-[Hyp3,Thi5,D-Tic7,Oic8]-BK (Hoe140) (100 nM; n = 4). Contractile responses to bradykinin itself were partially, but significantly, inhibited by the B1 receptor-selective antagonist, [Leu8,des-Arg9]-BK (10 microM) (P < 0.05), or by the B2 receptor-selective antagonist Hoe140 (100 nM) (P < 0.005) alone, and were largely blocked by a combination of the two antagonists (P < 0.0001). 4. The combined presence of the carboxypeptidase inhibitor DL-2-mercaptomethyl-3-guanidinoethylthiopropanoicacid (mergetpa; 10 microM), the neutral endopeptidase inhibitor, phosphoramidon (1 microM),and the angiotensin-converting enzyme inhibitor, enalaprilat (1 microM) increased the potency of bradykinin17 fold (P<0.001), but that of [des-Argl-BK was unchanged (P>0.05): pD2 estimates were 7.6 +/- 0.1 and 6.8 +/- 0.1 for bradykinin and [des-Argl-BK, respectively, in treated preparations. In the presence of peptidase inhibitors, the affinities of the antagonists [Leu8,des-Arg9]-BK and [des-Arg'j-Hoel4O were unchanged as compared with those determined in the absence of peptidase inhibitors (P> 0.05).[Leu8,des-Argj-BK inhibited responses to bradykinin under these conditions (n = 4).5. In endothelium-denuded preparations of the rabbit isolated aorta, an archetypal B1 receptor preparation,contractile responses to the B1 receptor-selective agonist [des-Argl-BK (10nM- 1O0 AM) (and to bradykinin) increased progressively with time of tissue incubation; and [des-Argl-BK responses were completely antagonized by the B. receptor antagonist [Leu8,des-Arg9]-BK (pKB 6.3 +/- 0.2; n = 13).6. In experiments measuring stimulation of hydrolysis of phosphatidylinositol in rabbit urinary bladder,[des-Argl-BK (10 microM- 1 mM), and bradykinin (100 microM) significantly increased accumulation of inositol phosphates (P<0.0001). The increase in accumulation of inositol phosphates evoked by [des-Arg9]-BK(10 microM - 1 mM) was significantly inhibited by [des-Arg'j-Hoe 140 (10 microM) (P <0.01).7. We conclude that in the mucosa-free rabbit urinary bladder, [des-Argl-BK evokes contraction largely via activation of B1 receptors which have similar properties, including time-dependent induction,to B1 receptors in the rabbit isolated aorta. Bradykinin evokes contraction via stimulation of both B1 and B2 receptors, but does not require conversion by peptidases in order to activate B1 receptors. We demonstrate, for the first time, B1 receptor-coupling to phosphatidylinositol hydrolysis in an intact tissue preparation.

Amino Acid Sequence↗

PubMed1995

Subtypes of endothelin ETA and ETB receptors mediating tracheal smooth muscle contraction.

In the isolated rabbit trachea, endothelin (ET)-1, ET-3 and the selective ETB receptor agonists, IRL 1620 and sarafotoxin S6c (STXc), induced contraction with EC50 of 2-9 nM. An ETA1 receptor antagonist, BQ-123, was ineffective whereas desensitization of the ETB receptor strongly antagonized the effect of ET-3, IRL 1620 and STXc. An ETB1 receptor antagonist, RES-701-1, antagonized the effects of ET-3 and IRL 1620 whereas the effect of STXc was antagonized by an ETB2 receptor antagonist, BQ-788. In the ETB-desensitized trachea, only ET-1 induced large contraction that was partially antagonized by BQ-123. These results suggest that ET induces tracheal contraction by activating multiple ET receptors: the ET-1-selective ETA (BQ-123-sensitive ETA1 and insensitive ETA2 subtypes) and the isopeptide-nonselective ETB receptors (RES-701-1-sensitive ETB1 and insensitive ETB2 subtypes).

Animals↗

PubMed2002

Receptor-mediated modulation of avian caecal muscle contraction by melatonin: role of tyrosine protein kinase.

Abstract: Melatonin receptors in the quail caecum were studied by 2[125I]iodomelatonin binding assay and the involvement of tyrosine protein kinase in the melatonin-induced contraction was explored. The binding of 2[125I]iodomelatonin in the quail caecum membrane preparations was saturable, reversible and of high affinity with an equilibrium dissociation constant (Kd) of 24.6 +/- 1.1 pm (n = 7) and a maximum number of binding sites (Bmax) of 1.95 +/- 0.09 fmol (mg/protein) (n = 7). The relative order of potency of indoles in competing for 2[125I]iodomelatonin binding was: 2-iodomelatonin > melatonin > 2-phenylmelatonin > 6-chloromelatonin > 6-hydroxymelatonin > N-acetylserotonin, indicating that ML(1) receptors are involved. The binding was inhibited by Mel1b melatonin receptor antagonists, luzindole and 4-phenyl-2-propionamidotetralin (4-P-PDOT) as well as by non-hydrolyzable analogs of GTP like GTPgammaS and Gpp(NH)p but not by adenosine nucleotides. The latter suggests that the action of melatonin on the caecum is G-protein linked. Cumulative addition of melatonin (1-300 nM) potentiated both the amplitude and frequency of spontaneous contractions in the quail caecum. The potentiation of rhythmic contractions was blocked by both luzindole and 4-P-PDOT. Antagonists of tyrosine kinase, genistein(2 microM) and erbstatin(4 microM) suppressed the modulation of spontaneous contractions by melatonin, but not inhibitors of protein kinase C (PKC) or protein kinase A (PKA). Melatonin-induced increment in spontaneous contraction was blocked by nifedipine (0.4 nM). Thus, we suggest that melatonin potentiates spontaneous contraction in the quail caecum via interacting with G-protein-coupled Mel(1b) receptor which may activate L-type Ca2+ channels by mobilizing tyrosine kinases.

1-(5-Isoquinolinesulfonyl)-2-Methylpiperazine↗

PubMed2002

[Calcium regulation by troponin and its genetic disorder in striated muscle contraction].

Contraction of skeletal and cardiac muscles is regulated by Ca2+ through specific Ca(2+)-regulatory proteins, troponin and tropomyosin, located in the thin filament. Troponin is a Ca2+ receptive protein consisting of three differet components, troponins C, I, and T. The essential mechanisms of Ca(2+)-regulation are the inhibition of contractile interaction between myosin and actin by the inhibitory action of troponin I and the reversal of the inhibition by troponin I through the Ca(2+)-binding to troponin C. All three components of troponin are required for the Ca(2+)-regulation of contraction. This article reviews following aspects of troponin researches: 1) early studies on the structure and function of troponin, 2) molecular mechanisms of Ca(2+)-regulation, 3) principles of troponin-exchange in skinned fibers and properties of troponin isoforms thereafter clarified under physiological conditions, 4) recent studies on the functional consequences of the mutations in human cardiac troponins T and I that cause genetic disorders, familial hypertrophic cardiomyopathy (HCM), and familial dilated cardiomyopathy (DCM).

Calcium↗

PubMed1982

An in vivo procedure for estimating spasmolytic activity in the rat by measuring smooth muscle contractions to topically applied acetylcholine.

An in vivo procedure for evaluating potential organ selectivity of spasmolytics has been developed. This involves the determination of comparative potencies, expressed as DR10 of spasmolytics against contractions induced by topical application of acetylcholine on rat colon, rectum and urinary bladder. Experiments with two well known spasmolytics, namely N-butyl-scopolammonium bromide and dicyclomine HCl yielded results consistent with data reported in the literature. This procedure provides a rapid, inexpensive and rather accurate estimate of organ selectivity of spasmolytics.

Acetylcholine↗

PubMed1981

Depression of nerve-mediated smooth muscle contractions in vitro by plasma of an anephric rabbit and uremic patients.

Isolated hypogastric nerve-vas deferens preparations from guinea pigs pigs were used in vitro to detect effects of plasma solutes from a nephrectomized rabbit or uremic patients on nerve-mediated contractions. Plasma collected from the subjects was ultrafiltered and applied directly to the tissue in an organ-bath at 34-36 degrees C. Plasma solutes with molecular weights (M.W.) smaller than 500 depressed contractions, their potency being greater when derived from the anephric rabbit and from patients than from the healthy control. Plasma solutes with a M.W. of 500-10,000 from the healthy rabbit augmented contractions, whereas those from the anephric rabbit depressed them. Human plasma solutes with a M.W. of 500-5,000 or 5,000-10,000 exhibited no effect except a slight depression by those with a M.W. of 500-5,000 from uremic patients. High M.W. plasma solutes (10,000-20,000 daltons) from the patients were also found to depress contractions more strongly than those from healthy men. It is concluded that uremic metabolites capable of depressing peripheral autonomic functions accumulate in the nephrectomized rabbit and in patients with renal failure, and the degree of depression varies with the difference in M.W. of the metabolites.

Animals↗

PubMed1978

Effects of the beta-receptor antagonists propranolol, oxprenolol and labetalol on human vascular smooth-muscle contraction.

1. Spiral strips of human digital arteries have been studied in vitro to investigate whether DL-propranolol, D-propranolol, oxprenolol and labetalol have peripheral vascular effects in man. 2. Labetalol was a potent inhibitor of contractile responses to noradrenaline, but had less effect on responses to 5-hydroxytryptamine and barium chloride. 3. DL-and D-propranolol were equally effective inhibitors of responses to barium chloride. They were only weak antagonists of noradrenaline responses, but stronger, non-competitive antagonists of 5-hydroxytryptamine responses. 4. Oxprenolol was only a weak inhibitor of the responses to both noradrenaline and 5-hydroxytryptamine and had little effect on responses to barium chloride. 5. It is concluded that labetalol has specific alpha-adrenoreceptor-blocking properties, which are probably relevant to its therapeutic action in man. Propranolol has non-specific inhibitory effect on vascular smooth muscle, which might contribute to its hypotensive activity at high concentrations, but oxprenolol has only slight peripheral effects that are probably therapeutically insignificant.

Adrenergic beta-Antagonists↗

PubMed1992

Transient responses of heart rate, skin and muscle sympathetic nerve activity before and after anticipatory muscle contraction.

Sympathetic nerve activity leading to skin (SSA) and skeletal muscle (MSA) and heart rate were measured before and during two-minute static handgrip (SHG) in seven healthy volunteers. Two different situations were set before commencement of the exercise; one was that a preparation time of between 4 and 6 minutes was set prior to SHG while no information of starting time for exercise was given to the subjects (Cond. 1). Another was that after two minutes of control rest, countdown was started two minutes before SHG and then the handgrip was started (Cond. 2). Heart rate for 10-s before SHG in Cond. 2 increased significantly from the control value, while there was no significant change in Cond. 1. The magnitude of heart rate response to SHG was the same in either condition. Although SSA for 10 seconds just before the exercise did not show any change from the control value in Cond. 1, it increased in Cond. 2. There was no difference in SSA response patterns during SHG in either condition. Before commencement of SHG, MSA was suppressed at 10-s before exercise from the control value in Cond. 2, but there was no significant change in Cond. 1. After onset of contraction, MSA was suppressed in the brief initial period regardless of countdown, thereafter MSA increased time-dependently. The MSA response pattern to SHG was almost identical in both conditions.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

PubMed2006

Uropathogenic Escherichia coli alters muscle contractions in rat urinary bladder via a nitric oxide synthase-related signaling pathway.

BACKGROUND: Uropathogenic Escherichia coli (UPEC) is a common cause of urinary-tract infection. The mechanisms by which bacteria cause the symptoms of cystitis remain unclear. METHODS: The contractions of isolated rat detrusor strips evoked by electrical field stimulations (EFS) or by exogenous agonists and immunoblotting for the detection of protein expression in the bladder were measured in the short (1 h) and long (24 h) term after the intravesical instillation of J96 (O4:K6) strain or UPEC isolated from patients with acute E. coli pyelonephritis or E. coli lipopolysaccharide (LPS). RESULTS: One hour after the instillation of UPEC, the level of endothelial nitric oxide synthase (eNOS) and the contractile response, but not protein kinase C (PKC) and extracellular signal-regulated kinase (ERK)-1/2 activation, were higher. Twenty-four hours after UPEC treatment, detrusor contractions were decreased, and inducible (i) NOS protein expression and ERK1/2 phosphorylation, but not PKC activation, were observed. Both aminoguanidine and PD98059 treatment markedly reversed the decrease of EFS- and acetylcholine-evoked detrusor contractions induced by UPEC. The instillation of LPS triggered PKC activation but not ERK1/2 phosphorylation. CONCLUSIONS: Short-term intravesical instillation of UPEC enhances detrusor contractions through an eNOS-related pathway, but iNOS-regulated ERK1/2 signaling may be involved in long-term UPEC treatment-induced responses. There are different mechanisms involved in the responses induced by UPEC and LPS.

Animals↗

PubMed1990

The theory of sliding filament models for muscle contraction. II. Biochemically-based models of the contraction cycle.

A seven-state sliding filament model is proposed which differs from the model of Eisenberg & Greene. It is based on a simplified version of the in-vitro contraction cycle of Stein et al., and also has some desirable dynamical features of the empirical three-state model of Nishiyama & Murase. Appropriate x-dependences for all reaction rates are derived from the transition-state theory. The seventh-state is assumed to be a high-tension intermediate of A.M.ATP, from which direct but x-dependent dissociation can occur. If the final A.M.ATP state has a sufficiently lower tension than that of A.M.ADP.Pi, then the dominant escape path from the intermediate state is shown to be direct dissociation of the actin-myosin bond. This leads to an approximate five-state model for active and relaxed muscle in which A.M and the final A.M.ATP state are omitted.

Actins↗

PubMed2000

Non-invasive approach of motor unit recording during muscle contractions in humans.

Information about the structural and functional characteristics of the motor unit (MU) is highly relevant for the diagnosis of neuromuscular disorders. Electromyography (EMG) is a suitable method for obtaining the information needed. The problem is the separation of the activity of one MU from others which are simultaneously active. Such investigations of single MU activity have commonly used invasive methods, e.g. employing a needle or a wire. Conventional surface-EMG methods have limited resolution and detect, at high contraction levels, multiple MU superimposed one on the other. The separation of the activity of a single MU can be achieved in a non-invasive way when highly specialised acquisition techniques are used. One approach, called high spatial resolution EMG (HSR-EMG), is based on the use of multi-electrode arrays in combination with a two-dimensional Laplace filter. The HSR-EMG permits the completely non-invasive detection of single MU activity even during maximal voluntary contractions. First applications have shown that the method provides a deeper insight into the functional and structural characteristics of the MU. In this paper the application of HSR-EMG to the diagnosis of neuromuscular disorders will be presented, and the latest results will be given of its application in the evaluation of treatment of patients with plexus lesion.

Electromyography↗

PubMed2003

Familial hypertrophic cardiomyopathy-linked alterations in Ca2+ binding of human cardiac myosin regulatory light chain affect cardiac muscle contraction.

The ventricular isoform of human cardiac regulatory light chain (HCRLC) has been shown to be one of the sarcomeric proteins associated with familial hypertrophic cardiomyopathy (FHC), an autosomal dominant disease characterized by left ventricular and/or septal hypertrophy, myofibrillar disarray, and sudden cardiac death. Our recent studies have demonstrated that the properties of isolated HCRLC could be significantly altered by the FHC mutations and that their detrimental effects depend upon the specific position of the missense mutation. This report reveals that the Ca(2+) sensitivity of myofibrillar ATPase activity and steady-state force development are also likely to change with the location of the specific FHC HCRLC mutation. The largest effect was seen for the two FHC mutations, N47K and R58Q, located directly in or near the single Ca(2+)-Mg(2+) binding site of HCRLC, which demonstrated no Ca(2+) binding compared with wild-type and other FHC mutants (A13T, F18L, E22K, P95A). These two mutants when reconstituted in porcine cardiac muscle preparations increased Ca(2+) sensitivity of myofibrillar ATPase activity and force development. These results suggest the importance of the intact Ca(2+) binding site of HCRLC in the regulation of cardiac muscle contraction and imply its possible role in the regulatory light chain-linked pathogenesis of FHC.

Adenosine Triphosphatases↗

PubMed1983

Alterations in smooth muscle contraction kinetics during tonic activation.

The kinetics of actin myosin interaction were studied in rat tracheal smooth muscle by analyzing the time course of post-vibration tension recovery. Longitudinal vibration (100 Hz sinus: 8% of the muscle length) of the contracted preparation (electrical field stimulation 30 Hz, 0.3 ms or 0.1 mM acetylcholine treatment) inhibits the process of force generation. The tension recovery after cessation of vibration follows a double exponential function with an initial fast and a subsequent slow component (the time constants averaged 1.17 +/- 0.10 s and 7.0 +/- 0.32 s (n = 60), respectively). Changes in the amplitude of vibration, the stimulation strength, or the extent of resting tension affect the amplitude without altering the time constants of tension recovery. These experimental conditions influence rather the number than the kinetics of acting cross-bridges. An extension of the pre-vibration stimulation period from 15 s to 16 min as well as a reduction in temperature from 37 degrees C to 25 degrees C hardly affects the extent of force development. However, the time constants of both the fast and the slow component of tension recovery were increased by up to a factor of about 7. These experimental results indicate an effect on the kinetics of actin myosin interaction.

Actins↗

PubMedDate not supplied

[Effect of calcium on the temporal characteristics of muscle contraction].

It is shown that the shape of mechanical relaxation time spectrum of single glycerinated rabbit fibre m. psoas changed with calcium concentration. When increasing Ca++ of the rate constant of delayed tension development increases several times in the absence of inorganic phosphate. Addition of 10 mM of inorganic phosphate increases this rate constant and sharply decreases its calcium dependence. These data are discussed in terms of possible connection between cross-bridges by means of ATPase reaction product-inorganic phosphate.

Adenosine Triphosphatases↗

PubMed2004

Muscle contractions and auditory perception in tinnitus patients and nonclinical subjects.

Evidence has been accumulating linking subjective tinnitus to the somatosensory system. Most subjective tinnitus patients can change the psychoacoustic attributes of their tinnitus with forceful head and neck contractions. This study assessed the significance of such somatic modulation of tinnitus by testing nonclinical subjects. Like tinnitus patients, about 80% of nonclinical subjects, who had ongoing tinnitus at the time of testing (whether or not they were previously aware of it), could modulate their tinnitus with head and neck contractions. Over half of those with no tinnitus at the time of testing could elicit a tinnitus-like auditory perception with head and neck contractions. The finding that forceful head and neck contractions, as well as loud sound exposure, were significantly more likely to modulate ongoing auditory perception in people with tinnitus than in those without tinnitus supports the concept of a neural threshold for tinnitus. Somatic influences upon auditory perception are not limited to tinnitus sufferers but appear to be a fundamental property of the auditory system.

Acoustic Stimulation↗

PubMed1978

Inhibitory action of prostaglandin E1 on smooth muscle contraction and calcium responses.

The relation between the inhibitory action of prostaglandin (E1 (PGE1) and external Ca concentration was investigated using the guinea-pig isolated ureter and the perfused central artery of the rabbit isolated ear. PGE1 20 ng/ml reduced the ureteral contraction evoked by a single electrical stimulation. This inhibitory action of PGE1 was enhanced with a decreased external Ca concentration. PGE1 100 ng/ml also reduced Ca-induced contracture of the ureter depolarized in Ca-free K(80 mM)-Krebs' solution. Furthermore, PGE1 50 ng/ml inhibited the responses of peripheral vascular resistance to noradrenaline, and this effect increased with a reduced external Ca concentration.

Animals↗

PubMed1995

Possible mechanism to induce protein kinase C-dependent arterial smooth muscle contraction after subarachnoid haemorrhage.

A possible mechanism for the induction of protein kinase C (PKC)-dependent vascular contraction independent to the increase of intracellular Ca++ was investigated in the pathogenesis of cerebral vasospasm in the double subarachnoid haemorrhage (SAH) model. The level of 1,2-diacylglycerol (DAG), which is an intrinsic PKC activator, significantly increased from days 4 to 7 in the basilar artery after the initial SAH, and the continuous administration of 1,2-bis(nicotinamido)-propane (AVS), a novel free radical scavenger, not only lowered the concentration of lipid peroxides in the CSF but also successfully suppressed the basilar arterial wall in the same model. It was suggested that lipid peroxides generated in the subarachnoid clot affect the DAG content of the cerebral artery. Analysis of hydroxy-eicosatetraenoic acids (HETEs) with high performance liquid chromatography (HPLC) revealed the production of relatively large amount of 12-HETE in the subarachnoid clot. To examine the potential effect of exogenous 12-HETE on the DAG content of the cerebral artery, the basilar artery was incubated with 12-HETE in vitro. 12-HETE induced a concentration-dependent slow increase in DAG content in the arterial wall after 6 hours of incubation. Under conditions in which DAG formation was facilitated by the Ca(++)-ionophore, DAG accumulation in the basilar artery was enhanced in the presence of 12-HETE. It was suggested that 12-HETE generated in the subarachnoid clot, induced DAG accumulation in the arterial wall by inhibition of DAG metabolism, resulting in the induction of prolonged PKC-dependent smooth muscle contraction in the pathogenesis of cerebral vasospasm.

12-Hydroxy-5,8,10,14-eicosatetraenoic Acid↗

PubMed1995

Chronic hypoxia impairs pulmonary venous smooth muscle contraction.

Chronic hypoxia increases total pulmonary vascular resistance and causes pulmonary hypertension. Although the effect of chronic hypoxia on pulmonary arterial tissue has been extensively studied, very little is known about the effects on the pulmonary vein. The purpose of the present investigation was to determine the effect of chronic hypoxia on pulmonary venous reactivity to several vasoactive agonists and on the venous response to acute hypoxia. Isolated pulmonary venous rings were taken from rats exposed to 2, 7, and 14 days of hypoxia (FIO2 = 0.1). A decrease in the response of the pulmonary vein to KCl was observed after 14 days of hypoxia. The reactivity (maximum active force produced) of the pulmonary vein in response to phenylephrine (PE) was reduced after 7 days of hypoxia. The response of the pulmonary vein to angiotensin II (AII) was more sensitive to the effects of chronic hypoxia since decreased reactivity to angiotensin II occurred after only 2 days of hypoxia. Prolonged hypoxia (14 days) had no further effect on the decreased reactivities to PE and AII. The sensitivities of pulmonary venous muscle to PE and AII were decreased (increased ED50 values) by 2 days of chronic hypoxia, but tended to return to control levels after 7 and 14 days of hypoxia. However, the contractile response of the pulmonary vein to acute hypoxia was not changed even after 14 days of chronic hypoxia. These results suggest that chronic hypoxia: (1) impairs pulmonary venous smooth muscle contractility; (2) reduces pulmonary venous reactivity and sensitivity to phenylephrine and angiotensin II; and (3) does not alter the pulmonary venous contractile response to acute hypoxia.

Angiotensin II↗