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At least 1,171 records · Page 65Linked to original sources
PubMed1990

Evidence for generation of a large amount of nitric oxide-like vascular smooth muscle relaxant by cholesterol-rich neutrophils.

To determine the effect of cholesterol incorporation on the ability of neutrophils to generate superoxide radicals and nitric oxide-like vasorelaxant material, isolated human neutrophils were incubated with cholesterol-rich liposomes, which increased total cholesterol content by 141% and esterified cholesterol content by 523%. Cholesterol loading resulted in 5 to 7 fold increase in cytosolic calcium in resting as well as in PMA or f-MLP-stimulated cells, but a marked (P less than 0.01) reduction in both PMA- and f-MLP-stimulated superoxide radical generation by these cells. Nitric oxide-like activity measured as relaxation of rat aortic rings was more pronounced (P less than 0.02) in cholesterol-rich than in cholesterol-poor cells. The greater relaxation of aortic rings in response to cholesterol-rich neutrophils was observed in rings with or without intact endothelium, and was potentiated by superoxide dismutase and inhibited by oxyhemoglobin as well as L-NMMA, thus suggesting that the vasorelaxant material was nitric oxide. The greater generation of nitric oxide by cholesterol-rich neutrophils occurs perhaps in response to increased cytosolic calcium.

Animals↗
PubMed1978

[Kinetics of guinea pig taenia coli smooth muscle relaxation. Effect of papaverine and polarization].

Experiments were conducted on isolated strips of the guinea pig taenia coli by the double sucrose gap technique. The effect of papaverins on the relaxation kinetics of the polarized and depolarized smooth muscle after contractions induced by electric stimulation was investigated. Depolarized muscle was stimulated by long-lasting hyperpolarizing pulses; contraction arose in response to the termination of the current pulse (off-response). It was found that: 1) the relaxation phase of the depolarized muscle off-response was slowed down as compared with the relaxation phase of the spontaneous contractions in Krebs solution; 2) papeverine accelerates the relaxation phase of the off-response of the depolarized muscle; 3) papaverine does not accelerate the relaxation phase of the evoked contractions in Krebs solution; 4) hyperpolarization and additional depolarization accelerate the relaxation phase of the off-response of the depolarized muscle; 5) hyperpolarization does not accelerate the relaxation phase of the off-response of the depolarized papaverine-treated muscle. The data obtained suggest the existence of the slow electroexcitable calcium channels in the membrane of the smooth muscle cells blocked by papaverine. The calcium influx through these channels slows down the relaxation phase of the depolarized muscle off-response.

Animals↗
PubMed2006

Clinical observations on the use of the muscle relaxant rocuronium bromide in the dog.

This study was designed to evaluate the effectiveness of neuromuscular blockade with rocuronium bromide (rocuronium) in eighty dogs anaesthetised for a variety of surgical procedures. Rocuronium 0.3 or 0.6 mg/kg (G03 and G06) was administered intravenously (IV) and neuromuscular function was monitored with an acceleromyograph. Lag time (LT) was >1 min in both groups. Onset time (OT) was 2+/-0.9 and 1.1+/-0.6 min in the groups given 0.3 and 0.6 mg/kg, respectively. There was a significantly longer time of action with 0.6 mg/kg in contrast to 0.3 mg/kg rocuronium. Time of no response (TonR) was 9.1+/-4.9-16.9+/-6.1 min in the groups given 0.3 and 0.6 mg/kg, respectively. The time from the end of injection until 25% recovery of the first twitch from the baseline value (T1(25)) was 13.8+/-5.5 and 22.3+/-6.7 min in the groups given 0.3 and 0.6 mg/kg, respectively. T1(25-75) was similar in both groups. Total recovery to baseline values was achieved in 23.8+/-6.6 and 31.9+/-6.5 min in the groups given 0.3 and 0.6 mg/kg, respectively (P<0.05). Premedication, maintenance agent, body position and stimulation site had no significant influence on the pharmacodynamic parameters in both groups. It was concluded that rocuronium is an effective non-depolarising muscle relaxant in the dog under clinical conditions.

Androstanols↗
PubMed1986

Interference of phorbolesters with endothelium-dependent vascular smooth muscle relaxation.

Histamine-induced endothelium-dependent relaxation (EDR) in the pulmonary artery was inhibited in a concentration-dependent manner by the phorbolester phorbol 12,13-dibutyrate (PDBu) (IC50: 70 nM) whereas EDR occurring in response to ionophore A 23187 was not affected by PDBu. The phorbolester 4 alpha-phorbol 12,13-didecanoate (4 alpha-PDD), which does not activate protein kinase C (PKC), was without effect on receptor- or ionophore-induced EDR. The observed inhibition of signal transduction by PKC activation is suggested to reflect phosphorylation of the GTP binding protein Ni.

Animals↗
PubMed1988

Pharmacology of natural compounds. I. Smooth muscle relaxant activity induced by a Ginkgo biloba L. extract on guinea-pig trachea.

A standardized Ginkgo biloba L. extract containing flavonol glycosides induces a concentration-dependent relaxation of guinea-pig trachea in vitro and antagonizes in vivo bronchoconstriction induced by various agonists. The action of the extract appears to be mediated partially by an interaction with the eicosanoid system particularly through specific stimulation of the PGE2 biosynthesis and partially by beta-adrenoceptor activation. The relaxation of guinea-pig trachea induced by the extract is in fact antagonized by indomethacin (2 x 10(-8)M), ETYA (3.4 x 10(-8)M) and sotalol (4 x 10(-6)M). The concentration-response curves obtained with tracheal preparation from reserpinized guinea-pig and those performed in the presence of a glutathione depletor (CDNB 1 x 10(-5)M) are modified in a similar manner confirming that the extract can act on both the systems: adrenergic as well as prostaglandinergic.

5,8,11,14-Eicosatetraynoic Acid↗
PubMed1990

Protease inhibitors potentiate smooth muscle relaxation induced by vasoactive intestinal peptide in isolated human bronchi.

To examine the role of endogenous proteases in limiting the bronchodilating effects of vasoactive intestinal peptide (VIP) in human airway, we studied precontracted bronchial rings from five nonsmokers undergoing heart-lung transplantation for pulmonary hypertension, either primary or secondary to congenital heart disease. The protease inhibitors aprotinin, leupeptin, phosphoramidon, and soybean trypsin inhibitors significantly potentiated the bronchodilator response to VIP. Even in the presence of the four protease inhibitors, VIP-induced bronchodilation reversed spontaneously in some tissues. These studies show that degradation by endogenous airway proteases is an important determinant of the bronchodilating potency of VIP in isolated human airway.

Adolescent↗
PubMed1996

Vascular smooth muscle relaxation by alpha-adrenoceptor blocking action of dobutamine in isolated rabbit aorta.

We investigated the mechanism of vascular relaxation produced by dobutamine, a positive inotropic agent with beta 1-adrenergic action. Dobutamine concentration-dependently (10 nM-10 microM) relaxed ring segments of rabbit aorta partially precontracted with 1 microM phenylephrine (PE) but did not relax those precontracted with 40 mM K+ or 5 microM prostaglandin F2 alpha (PGF2 alpha). The relaxation was not completely inhibited by pretreatment with 10 microM propranolol. Dobutamine did not significantly increase tissue cyclic AMP levels concomitantly with relaxation as does isoproterenol (ISO) in rabbit aorta. Dobutamine produced a parallel rightward shift in concentration-response curves to PE. The Schild plot analysis resulted in a linear regression of a slope of 1.077 +/- 0.077, which was not significantly different from unity. The pA2 value of dobutamine as compared with PE in rabbit aorta was 6.81 +/- 0.03. Dobutamine causes arterial dilatation mediated not only through a beta-adrenergic action but also through an alpha-adrenergic blocking action in rabbit aorta.

Abortifacient Agents↗
PubMed1989

Vascular effects of propofol: smooth muscle relaxation in isolated veins and arteries.

Isolated hepatic portal veins and aorta taken from the rat were used to investigate the direct action of the intravenous anaesthetic propofol. This compound is known to produce a fall in blood pressure in man and animals and it has been suggested that the hypotension may result from a direct vasodilator action on the veins and arterioles. In our experiments propofol caused a dose related decrease of potassium-induced tone in both types of blood vessel. However, the concentrations required to produce this effect in the experiments on veins were significantly lower than those required to produce similar changes in the isolated artery preparation. We conclude that this direct action may contribute towards the hypotensive effects of propofol.

Animals↗
PubMed1995

Prodrugs of nitroxyl as potential aldehyde dehydrogenase inhibitors vis-a-vis vascular smooth muscle relaxants.

The synthesis and the chemical/biological properties of N-hydroxysaccharin (1) (2-hydroxy-1,2-benzisothiazol-3(2H)-one 1,1-dioxide), a nitroxyl prodrug, are described. When treated with 0.1 M aqueous NaOH, 1 liberated nitroxyl (HN=O), a known inhibitor of aldehyde dehydrogenase (AlDH), in a time-dependent manner. Nitroxyl was measured gas chromatographically as its dimerization/dehydration product N2O. Under these conditions, Piloty's acid (benzenesulfohydroxamic acid) also gave rise to HNO. However, whereas Piloty's acid liberated finite quantities of nitroxyl when incubated in physiological phosphate buffer, pH 7.4, formation of nitroxyl from 1 was minimal. This was reflected in the differential inhibition of yeast AlDH (IC50 = 48 and > 1000 microM) and the differential relaxation of preconstricted rabbit aortic rings in vitro (EC50 = 1.03 and 14.0 microM) by Piloty's acid and 1, respectively. The O-acetyl derivative of 1, viz., N-acetoxysaccharin (13a), was much less active in both assays. It is concluded that N-hydroxysaccharin (1) is relatively stable at physiological pH and liberates nitroxyl appreciably only at elevated pH's. As a consequence, neither 1 nor its O-methyl (8a) and O-benzyl (8b) derivatives were effective AlDH inhibitors in vivo when administered to rats at 1.0 mmol/kg.

Aldehyde Dehydrogenase↗
PubMed1997

Mechanism of vascular smooth muscle relaxation by estrogen in depolarized rat and mouse aorta. Role of nuclear estrogen receptor and Ca2+ uptake.

17 beta-Estradiol induces vasodilation in vitro and in vivo, which has been suggested to contribute to the cardiovascular protection by this ovarian steroid hormone. However, the exact mechanism of vasorelaxation by estrogens remains to be elucidated. In this study, we analyzed the potential role of genomic mechanisms involving the nuclear estrogen receptor and inhibition of entry of extracellular Ca2+ in 17 beta-estradiol-induced vasorelaxation in depolarized aortic rings, isolated from male and female rats and male mice. In both male and female rat aortic rings without endothelium and in intact male mouse aortic rings treated with NG-nitro-L-arginine, 17 beta-estradiol caused dose-dependent (0.3 to 30 mumol/L) relaxation of contraction evoked by high-K+ depolarization (30 and 45 mmol/L KCl, respectively). The estrogen receptor antagonist ICI 164384 had no effect on 17 beta-estradiol-induced relaxations. 125I-17 beta-estradiol binding studies showed the presence of high-affinity cytosolic-nuclear estrogen receptors in control male mouse aortas. Comparable relaxations of aortic rings isolated from control and estrogen receptor-deficient transgenic mice provided direct evidence that the nuclear estrogen receptor is not involved in this response. 17 beta-Estradiol-induced relaxation of rat aortic rings could not be prevented by cycloheximide or actinomycin D, suggesting that the response was not mediated by de novo protein synthesis or gene transcription. In rat aortic rings, 17 beta-estradiol inhibited the increase of 45Ca uptake by 30 mmol/L KCl at concentrations (10 and 30 mumol/L) that caused vasorelaxation in the same tissue, suggesting that inhibition of Ca2+ entry contributes to the response. 17 alpha-Estradiol was less effective, and estrone was devoid of vasorelaxing activity. Vasorelaxation by estrogens in female and male rat aortas was similar, indicating no gender difference in vascular responses under these conditions.

Action Potentials↗
PubMed1994

Selective pulmonary and venous smooth muscle relaxation by furosemide: a comparison with morphine.

Furosemide and morphine reduce pulmonary edema associated with congestive heart failure. It is uncertain whether furosemide or morphine are direct-acting relaxants of arterial and venous smooth muscle. The authors compared the effect of furosemide and morphine on isolated rings of canine pulmonary artery (PA) and vein (PV) and mesenteric, splenic and anterior tibial arteries and their corresponding veins precontracted with norepinephrine or (15S)-hydroxy-11 alpha, 9 alpha-(epoxymethano)prosta-5Z,13E-dienoic acid. Furosemide (10-300 microM) selectively relaxed veins by an endothelium-independent mechanism, with its greatest efficacy on the PV. Morphine (10-1000 microM) relaxed both arteries and veins. The mechanism of relaxation by furosemide and morphine was examined in the PV and PA. Morphine-induced relaxation of the PV and PA was dependent on prostanoid release from endothelium and smooth muscle because it was attenuated in endothelium-rubbed and ibuprofen-treated PV and PA but not in blood vessels treated with inhibitors of nitric oxide system/cyclic GMP system (I-NG-nitroarginine and methylene blue). Furosemide-mediated relaxation of the PV was refractory to each of these interventions. Similarly, furosemide- and morphine-induced relaxation of the PV were unaffected by 4-aminopyridine, tetraethylammonium, glibenclamide, dendrodotoxin and apamin and, thereby, were independent of an action on K+ channels. Reduction of extracellular K+ or Cl- attenuated furosemide-mediated relaxation of, and inhibition of 86Rb+ uptake by, PV even in the presence of ouabain. It was concluded that furosemide relaxes veins by an effect on Na+/K+/Cl- cotransport or chloride-mediated refilling of intracellular calcium stores.

Animals↗
PubMed1991

CGP 35348, a new GABAB antagonist, prevents antinociception and muscle-relaxant effect induced by baclofen.

1. CGP 35348, a new GABAB antagonist, was examined on antinociception induced by (+/-)-baclofen by use of the hot plate and writhing tests in mice and the paw pressure test in rats. CGP 35348 was also studied in mice on (+/-)-baclofen-induced impairment of rota-rod performance. 2. CGP 35348, injected either i.p. (60-100 mg kg-1 in mouse) or intracerebroventricularly (i.c.v.) (0.5-2.5 micrograms per mouse; 25 micrograms per rat) prevented (+/-)-baclofen-induced antinociception. 3. CGP 35348 did not modify oxotremorine- and morphine-induced antinociception in mice and rats. 4. CGP 35348 (2.5 micrograms i.c.v. per mouse) also prevented (+/-)-baclofen-induced impairment of the rota-rod test. 5. Two other GABAB antagonists, phaclofen (50 micrograms i.c.v. per mouse) and 2-OH-saclofen (2.5 micrograms-10 micrograms i.c.v. per mouse) did not modify (+/-)-baclofen-induced antinociception. 7. These results suggest that, at present, CGP 35348 is the only compound able to antagonize (+/-)-baclofen-induced antinociception.

Analgesics↗