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At least 1,621 records · Page 90Linked to original sources
PubMed2005

Intestinal dysmotility in inflammatory bowel disease: mechanisms of the reduced activity of smooth muscle contraction.

Inflammation suppresses intestinal motility, which secondarily induces abnormal growth of intestinal flora. Disturbance of this flora plays a role in the pathogenesis of mucosal inflammation, which in turn aggravates the intestinal dysmotility. Therefore, it is important to know the mechanism of alteration in motor function in the inflamed intestine. Recent studies have shown molecular mechanisms responsible for the motility disorder in the inflamed gut. These include an increase in the activity of myosin light-chain phosphatase and an alteration of ion channel activity in smooth muscle cells.

Animals↗
PubMed1989

The contracting muscle: a challenge for freeze-substitution and low temperature embedding.

Frog sartorius and semitendinosus muscles are quick-frozen either in the resting state or during contraction by means of a LN2 cooled falling copper block. The frozen specimens are freeze-substituted (acetone + OsO4 + uranyl acetate) in a REICHERT JUNG CS auto and either embedded in Spurr's resin and polymerised at a high temperature (60 degrees C) or embedded and polymerised in the Lowicryls K4M, K11M or HM23 at low temperatures (below -30 degrees C). Excellent morphological results are obtained when freeze-substitution, embedding and polymerisation are all carried out below -50 degrees C. Muscles in which a major portion of cellular K+ ions has been replaced by electron dense Cs+ or Tl+ ions are also cryofixed at rest or during contraction, freeze-substituted in pure acetone for 1 week at -80 degrees C and polymerised in K11M at -60 degrees C. A characteristic uneven distribution of the electron dense ions--known from earlier published control experiments--can be observed in sections of resting muscles. Electrically stimulated muscles show ion redistribution. It is concluded that freeze-substitution and low temperature embedding of quick-frozen contracting muscle may be used to investigate changes of ultrastructure, redistribution of cellular water and intracellular movements of mobile ions during muscle contraction.

Animals↗
PubMed1996

Enhancement of smooth muscle contraction with protein phosphatase inhibitor 1: activation of inhibitor 1 by cGMP-dependent protein kinase.

New method for purification of phosphatase inhibitor 1 (PPI-1) was developed which avoid the phosphorylation of PPI-1 during the purification and provides a high yield of highly pure preparation. Using this preparation, it was shown that PPI-1 was stoichiometrically phosphorylated by cGMP-dependent protein kinase at Thr-35 and the phosphorylated PPI-1 potently inhibited protein phosphatase 1. Addition of the phosphorylated PPI-1 to beta-escin-skinned single smooth muscle cells resulted in force development of the cells at the submaximal pCa2+. The results suggest that the phosphorylation of PPI-1 can be the mechanism for modifying the Ca2+ sensitivity of smooth muscle contractile response.

Amino Acid Sequence↗
PubMed1991

New reduced peptide bond substance P agonists and antagonists: effects on smooth muscle contraction.

Following the recent discovery of a new substance P (SP) competitive pancreatic acini cell receptor antagonist containing a reduced peptide bond in place of the C-terminal peptide bond, a new series of full chain and short chain (heptapeptide and hexapeptide) substance P analogues have been prepared in which one of the C-terminal-region peptide bonds has been replaced by CH2NH or CH2O groups. They were compared for their ability to recognize NK1 and/or NK2 tachykinin receptor binding sites on guinea pig ileum and rat duodenum smooth muscle preparations, respectively. It was found that all full sequence SP pseudopeptides were agonists with much reduced bioactivity in both tested systems and, in addition, [Gly9 psi(CH2NH)Leu10,Leu11]SP was found to be a relatively selective agonist for NK1 binding sites. Substitution of leucine at position 11 of SP heptapseudopeptides with phenylalanine generated a pseudopeptide with weak agonist activity when Gln at position 5 was replaced by D-Phe, or antagonists when this residue was replaced by D-Nal or D-Cpa. [Leu10 psi(CH2NH)Leu11]SP-(6-11) with Gln at position 6 substituted by D-Phe was a relatively stronger antagonist in both assay systems. These results suggest that, as with several other peptide systems of late, manipulation of the peptide bonds in SP can produce receptor antagonists which in some cases approach the potency of the classic spantide series and, furthermore, that the approach might be used to induce NK receptor specificity in both agonist and antagonist analogs.

Amino Acid Sequence↗
PubMed1993

Role of intracellular Ca2+ stores in smooth muscle contractions of the guinea pig vas deferens.

Guinea pig vas deferens was used as an animal model for alpha-1 adrenoceptor (alpha 1-receptor) mediated contractions in human hyperplastic prostatic tissue. The selective alpha 1-receptor agonist, phenylephrine (PE), induced fully reversible, dose-dependent contractions antagonized by increasing concentrations of the alpha 1-receptor blockers prazosin (1-100 nM) and YM 617 (0.1-10 nM). Removal of extracellular Ca2+ reduced PE-evoked contractions in a time-dependent manner. Nifedipine (1-1000 nM), a blocker of voltage-dependent L-type Ca2+ channels (VDCC), inhibited the PE-induced response by up to 65%. Removal of extracellular Ca2+ abolished the alpha 1-agonist reactivity in a time-dependent fashion. To elucidate the participation of intracellular Ca2+ stores in alpha 1-receptor-mediated contractions, the tissue was pretreated with ryanodine (10 microM) or thapsigargin (0.1 microM), established inhibitors of Ca2+ release from intracellular pools. Both substances reduced the PE contractions by up to 80%. Nifedipine suppressed the remaining contractions completely. This provides evidence that Ca2+ influx through VDCC and Ca2+ release from intracellular stores contribute to alpha 1-receptor-mediated contractions in the guinea pig vas deferens and may be important in obstructive benign prostatic hyperplasia.

Adrenergic alpha-Antagonists↗
PubMed1991

Effect of circulating factors on vascular smooth muscle contraction and its calcium uptake in uremia.

Uremia is often associated with alterations in calcium metabolism and vascular smooth muscle function in hypertension and atherosclerosis. The ways in which these conditions inter-relate are not clearly understood. In order to study the possibility that circulating factors might influence smooth muscle function, experiments were performed on rat aortic strips. The serum from both uremic patients and rats enhanced the norepinephrine-induced contraction (NEIC) and net 45-calcium uptake in rat aortic strips. In a similar manner, the serum of parathyroidectomized uremic rats also increased the NEIC, whereas verapamil reduced the aortic response to levels below those of the control, in the presence of uremic serum. These findings suggest that in both chronic (patients) and early (rats) stages of uremia, there is a circulating factor, different from parathyroid hormone, that affects calcium uptake and vascular smooth muscle contraction.

Adult↗
PubMed1988

Synthesis of some substituted quinazolinediones as potential inhibitors of smooth muscle contraction.

3-Substituted 2,4(1H,3H)-quinazolinediones were prepared from the corresponding N-substituted 2-aminobenzamides by treatment with ethyl chloroformate and KOH in ethanol. Also, a series of 3-substituted and 1-methyl-3-substituted 2,4(1H,3H)-quinazolinediones were synthesized by the reaction of 1-methyl-1,4-dihydro- and 1,4-dihydro-2,4-dioxo-3(2H)-quinazolineacetic acid with the corresponding N-substituted piperazines. The 13C NMR spectra and mass spectra of the compounds were measured and signals were assigned. Some of the compounds showed inhibitory action on contractile function of smooth muscle.

Animals↗
PubMed1976

Circulatory effects of isometric muscle contractions, performed separately and in combination with dynamic exercise.

Studies on central circulation and regional blood flow were performed in healthy male volunteers at rest, during sustained isometric forearm contraction at 20% of MVC, during dynamic leg exercise (100 W) and during combined isometric and dynamic exercise. In 10 subjects pulmonary oxygen uptake, arterio-venous oxygen difference, heart rate, leg blood flow and blood pressures in the pulmonary and subclavian arteries and in the right atrium were measured. In 4 of these subjects the temperature was measured in mixed venous blood and in subcutaneous tissue in an attempt to further analyse the blood flow distribution through central versus peripheral parts of the circulatory system. In 5 other subjects the splanchnic blood flow was estimated by hepatic vein catheterization and dye dilution technique at rest and during isometric forearm contraction. It was found that cardiac output, oxygen uptake, heart rate and arterial blood pressure all increased in response to isometric contraction. Quantitatively the changes in heart rate and cardiac output induced by a sustained contraction were more marked when the contraction was performed separately than when it was added to dynamic exercise. In spite of the increased arterial pressure, the leg blood flow did not increase significantly. Neither did the splanchnic blood flow increase in response to hand-grip contrmic exercise. Isometric exercise, however, caused a blood temperature fall and a rise in subcutaneous temperature indicating an increased blood flow through the skin. It is concluded that during sustained isometric muscle contraction 1. the blood flow increase is mainly distributed to peripheral circulatory areas, 2. a concomitant dynamic exercixe interferes with the circulatory adaptation only to a small extent.

Abdomen↗
PubMed2003

An x-ray diffraction study on early structural changes in skeletal muscle contraction.

Structural changes in frog skeletal muscle were studied using x-ray diffraction with a time resolution of 0.53-1.02 ms after a single electrical stimulus at 8 degrees C. Tension began to drop at 6 ms (latency relaxation), reached a minimum at 8 ms, and then twitch tension developed. The intensity of the meridional reflection at 1/38.5 nm(-1), from troponin molecules on the thin filament, began to increase at 4-5 ms and reached a maximum at approximately 12 ms. The meridional reflections based on the myosin 43-nm repeat began to decrease when the tension began to develop. The peak position of the third-order myosin meridional reflection began to shift toward the higher angle at approximately 5 ms, reached a maximum shift (0.02%) at 10 ms, and then moved toward the lower angle. The intensity of the second actin layer line at 1/18 nm(-1) in the axial direction, which was measured at 12 degrees C, began to rise at 5 ms, whereas the latency relaxation started at 3.5 ms. These results suggest that 1), the Ca(2+)-induced structural changes in the thin filament and a structural change in the thick filament have already taken place during latency relaxation; and 2), the Ca(2+) regulation of the thin filament is highly cooperative.

Actins↗
PubMed1994

Preload release increases blood flow and decreases fatigue during repetitive isotonic muscle contractions.

The effects of preload on blood flow (Q), O2 uptake (VO2), and fatigue were investigated in the canine gastrocnemius-plantaris muscle in situ. Repetitive (1 contraction/s, 200 ms duration) afterloaded (0.25-0.3 maximal active isometric tension) isotonic tetanic contractions were performed in high-preload (HP; 69 g/g, n = 5), low-preload (LP; 35 g/g, n = 6), and preload-release (PR; 0 g/g, n = 5) experiments. Maximal Q values (1.0, 1.6, and 2.1 ml.min-1.g-1, P < 0.05 for all comparisons) and Q2 delivery (8, 13, and 17 mumol.min-1.g-1, P < 0.05 for all comparisons) increased significantly with decreasing preload. The maximal VO2 of HP was 7.2 mumol.min-1.g-1, which is significantly lower than both LP (10.5 mumol.min-1.g-1, P < 0.05) and PR values (11.4 mumol.min-1.g-1, P < 0.05); these differences were sustained through 20 min of contractions. Fatigue, measured as a loss of power production, was 63, 37, and 23% at 20 min of contractions in HP, LP, and PR, respectively, indicating significantly less fatigue with decreasing preload (P < 0.05 for all comparisons). These data demonstrate that the preload, present as the level of passive tension maintained between contractions, can influence Q, VO2, and fatigue during repetitive isotonic tetanic contractions of muscle in situ by a mechanically determined metabolic modulation of dynamic muscle performance.

Animals↗