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At least 1,171 records · Page 65Linked to original sources
PubMed1985

Detection and distribution of myosin isozymes in vertebrate smooth muscle.

Crude extracts of taenia coli (guinea-pig), gizzard (chicken), stomach, colon, ureter, bladder, mesenteric vein, mesenteric artery, uterus and vas deferens (dog) were electrophoresed under conditions which do not denature myosin (pyrophosphate gels). Two isozymes (G1 and G2) were observed in all cases. Their mobilities are the same in all organs, but there are some variations in their relative proportions. They have an ATPase activity. Based on electrophoretic mobility the light chains (L20 and L17) seem to be the same for both isozymes whilst the heavy chains are different. Isozyme G2 contains one type of heavy chain of an apparent molecular mass of 230 kDa, whilst isozyme G1 contains two types of heavy chains: one of apparent molecular mass of 230 kDa, and the other of apparent molecular mass of 200 kDa.

Adenosine Triphosphatases↗
PubMedDate not supplied

The contractile response of smooth muscle to immersion in hypertonic solutions.

1. Strips of bovine tracheal muscle and rabbit aorta produced sustained contractions on perfusion with Krebs solution made twice normal strength by addition of sucrose. The contractures were relaxed on return to normal Krebs solution. 2. Similar contractures were produced by tracheal muscle strips in Krebs solutions made twice normal strength by addition of galactose, glucose or NaCl whereas urea caused only a transient contraction. 3. In twice normal strength Krebs solution (sucrose added) the basal tension of rat portal vein and guinea-pig taenia coli was increased. Spontaneous mechanical activity was maintained, but the frequency of contractions was reduced. 4. The hypertonic contracture of bovine trachea in twice normal strength Krebs solution (sucrose added) was reduced by 15% by omission of Ca from the bathing fluid (0.1 mmol/l EGTA added). Severe Ca depletion, by prolonged washing in Ca-free Krebs with 12.5 mmol/l EGTA and Carbachol added, resulted in a 77% reduction in the hypertonic contracture. 5. In twice normal Krebs solution (sucrose added), the hypertonic contracture was partially relaxed by isoprenaline (4 x 10(-6) mol/l); the contractile response to carbachol was reduced; the contractile response to high-K Krebs solution was maintained. 6. Atropine (5 x 10(-7) mol/l) abolished the contractile response to carbachol, but had no effect on the hypertonic contracture. 7. It is suggested that the contraction of bovine tracheal strips in hypertonic solutions is mainly due to activation of the contractile myofilaments rather than simple cell shrinkage. Hypertonic solutions may also interfere with some steps in the excitation-contraction coupling sequence.

Animals↗
PubMed1987

Evidence that tracheal smooth muscle tone in guinea-pig is unaffected by overflow of noradrenaline released by perivascular nerve fibres.

1. Fluorescence histochemical techniques demonstrated that in the guinea-pig the cervical common carotid, cranial thyroid and caudal thyroid arteries were surrounded by a rich plexus of adrenergic nerve fibres. 2. The superior cervical ganglia were the source of the perivascular adrenergic fibres of the cranial thyroid arteries and the anterior half of the cervical common carotid arteries. These ganglia may also provide some of the perivascular adrenergic fibres of the caudal thyroid arteries. 3. Perivascular stimulation of the cranial thyroid and caudal thyroid arteries failed to elicit a response from isolated extrathoracic tracheal tube preparations. This suggests that it is unlikely that the guinea-pig extrathoracic trachealis muscle is innervated by adrenergic fibres arising from these perivascular plexuses or that overflow of noradrenaline from perivascular nerves causes dilatation of the trachealis muscle.

Animals↗
PubMed2004

Actions of R- and S-verapamil and nifedipine on rat vascular and intestinal smooth muscle.

1 We have investigated the actions of the calcium entry blockers nifedipine, R-verapamil and S-verapamil in rat aorta, colon and vas deferens. 2 In aorta and colon, these agents produced concentration-dependent relaxations of KCl (80 mM)-induced contractions. In both tissues, the order of potency was nifedipine > S-verapamil > R-verapamil. However, nifedipine showed selectivity for aorta (potency ratio, colon/aorta: 4.36), S-verapamil showed no selectivity (0.62), but R-verapamil showed selectivity for colon (0.19). 3 In prostatic portions of rat vas deferens, nifedipine (10 microM) abolished the contraction to a single electrical stimulus, but R- and S-verapamil were without effect. In epididymal portions of rat vas deferens, R- and S-verapamil inhibited alpha1-adrenoceptor-mediated contractions to a single electrical stimulus at concentrations of 10 microM and above. 4 In conclusion, R-verapamil may prove useful as an intestinal selective calcium entry blocker in the treatment of intestinal disease with a hypermotility component, e.g. irritable bowel syndrome.

Adrenergic alpha-1 Receptor Antagonists↗
PubMed1963

THE EFFECT OF PROSTAGLANDIN E1 ON RESPONSES OF SMOOTH MUSCLE TO CATECHOL AMINES, ANGIOTENSIN AND VASOPRESSIN.

Reduction of the pressor responses to adrenaline in the rabbit following administration of prostaglandin E(1) has been confirmed. The effect is, however, nonspecific since noradrenaline, angiotensin and vasopressin are also antagonized. Analogous responses were observed in blood flow experiments on the cat hind limb but not on the rabbit isolated auricles or the rabbit isolated duodenum. Contractions of the cat nictitating membrane produced by sympathetic preganglionic stimulation or by adrenaline were not decreased following injection of prostaglandin E(1) but the relaxation period was shorter. Contractions of the rabbit vas deferens induced in vivo by adrenaline were smaller after prostaglandin E(1) and this effect tended to be long-lasting.

Alprostadil↗
PubMed1989

The relaxant properties of human calcitonin gene-related peptide on vascular and extravascular capsular) smooth muscle of the isolated blood-perfused spleen of the anaesthetized dog.

1. The 37 amino acid human calcitonin gene-related peptide (CGRP), was injected intra-arterially into the isolated, blood perfused spleen of the dog. 2. The only vascular response observed to CGRP, once threshold had been reached (10-20 fmol), was a dose-dependent splenic arterial vasodilatation. 3. The mean intra-arterial bolus dose of CGRP to reduce the splenic arterial vascular resistance by 50% of maximum response was 0.52 +/- 0.12 pmol. This value was significantly lower than the ED50 for the non-selective beta-adrenoceptor agonist isoprenaline (P less than 0.01) in the same experiments. CGRP is the most potent splenic vasodilator yet tested. 4. The mean maximum vasodilator response to CGRP was significantly less (P less than 0.001) than that achieved with isoprenaline. 5. The time course of the splenic arterial vascular response to CGRP was substantially longer than that to isoprenaline. 6. The splenic vasodilator response to CGRP was not altered by the prior administration of the selective beta 2-adrenoceptor antagonist, ICI 118,551. 7. At all doses of CGRP that caused splenic vasodilatation there were substantial increases in spleen volume. The time course of the response and slope of the regression line suggested an active capsular relaxation component. 8. In view of its location within the spleen and high molar potency, CGRP may be considered as a potential factor in the local control of the circulation through the spleen.

Anesthesia↗
PubMed1996

Effects of adrenomedullin and calcitonin gene-related peptide on airway and pulmonary vascular smooth muscle in guinea-pigs.

1. The airway and pulmonary vascular effects of adrenomedullin were studied in the guinea-pig isolated trachea, main bronchi and pulmonary artery in vitro and compared to the effects of calcitonin gene-related peptide (CGRP). 2. In tracheal rings, CGRP (1 nM to 1 microM) potentiated the cholinergic contractions induced by electrical field stimulation (EFS) at 5 Hz in a concentration-dependent manner. At a concentration of 1 microM, CGRP slightly decreased the responses to log EFS frequency, producing 50% of the maximum contraction from a control value of 0.77 +/- 0.10 Hz to 0.54 +/- 0.05 Hz without a significant effect on the concentration-response curves to acetylcholine (ACh). In contrast, adrenomedullin (1 nM to 1 microM) did not alter either EFS-induced cholinergic or ACh-induced contractions. 3. In bronchial strips, CGRP (1 nM to 1 microM) slightly reduced both the non-adrenergic non-cholinergic (NANC) contraction induced by EFS at 10 Hz and the substance P (1 microM)-induced contraction in a concentration-dependent manner, whereas adrenomedullin (1 nM to 1 microM) was without effect. 4. Neither CGRP (1 microM) nor adrenomedullin (1 microM) altered NANC relaxation induced by EFS at 5 Hz in tracheal rings precontracted with histamine (10 microM). 5. Adrenomedullin (1 nM to 1 microM) and CGRP (1 nM to 1 microM) induced a concentration-dependent relaxation of the histamine (10 microM)- and prostaglandin F2 alpha (10 microM)-precontracted pulmonary arterial rings with intact endothelium with a similar potency. 6. Neither removal of the endothelium nor NG-nitro-L-arginine methyl ester (100 microM) altered the vasorelaxant effects of adrenomedullin (1 nM to 1 microM) and CGRP (1 nM to 1 microM). 7. The putative CGRP receptor antagonist, CGRP8-37 (1 microM to 10 microM) concentration-dependently attenuated the CGRP (3 nM to 30 nM)-induced vasorelaxant actions, whereas it had no effect on the relaxation of vessel rings induced by adrenomedullin (3 nM to 30 nM). 8. These results suggest that adrenomedullin is a potent vasodilator of the pulmonary artery without any bronchomotor effect in the guinea-pig lung, and that the vasorelaxant actions of adrenomedullin are not mediated via the activation of CGRP1 receptors.

Adrenomedullin↗
PubMed1992

Contractions induced by angiotensin I, angiotensin II and bradykinin in isolated smooth muscle from the human detrusor.

In isolated human detrusor preparations angiotensin (At)II 10(-9)-10(-5) M caused concentration-dependent contractions. The contractile effect was immediate, and had an amplitude which at the highest concentration used, 10(-5) M, reached 103 +/- 16% of the mean contraction produced by K+ 124 mM (27.6 +/- 1.4 mN). The AtII effect was completely blocked by saralasin 10(-6) M, but was not affected by pre-treatment of the preparations with captopril or enalaprilate. There was a marked tachyphylaxis to the actions of the peptide. AtI (10(-8)-10(-5) M) also caused contractions which were rapidly developing, and subject to a marked tachyphylaxis. At a concentration of 10(-5) M, the mean amplitude was 66 +/- 9% of the K(+)-induced contraction. The contractions were blocked by saralasin 10(-6) M, but not by captopril or enalaprilate 10(-5) M. In contrast, contractions produced by AtI in rabbit mesenteric arteries were practically abolished by the angiotensin converting enzyme (ACE) inhibitors. The contractions induced by both AtI and AtII were practically abolished after pre-treatment in a nominally calcium-free Krebs solution. However, blockade of L-type calcium channels by nifedipine 10(-6) M reduced the responses to both AtI 10(-6) M (by 38 +/- 4%) and AtII 10(-6) M (by 39 +/- 7%), but never abolished the contractions. Bradykinin (Bk; 3 x 10(-8)-10(-5) M) had a contractile effect in detrusor preparations which varied widely between strips. At a concentration of 3 x 10(-6) M, a maximum was reached amounting to 30 +/- 10% of the K(+)-induced contraction.(ABSTRACT TRUNCATED AT 250 WORDS)

Aged↗