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PubMed1988

The lack of involvement of cyclic nucleotides in the smooth muscle relaxant action of BRL 34915.

1. The relaxant effect of BRL 34915 has been examined on four isolated preparations, the bovine retractor penis (BRP), guinea-pig taenia coli, guinea-pig trachea and rabbit aortic strip contracted by either histamine, carbachol, noradrenaline or 10 mM KCl. Even though the probability of the involvement of external calcium entering through voltage-operated channels in these tissues varied, there was little corresponding variation in sensitivity to BRL 34915. 2. The relaxant effect of BRL 34915 on the BRP and guinea-pig taenia coli was unaffected by haemoglobin 3.3 microM or Apamin 0.5 microM, concentrations which blocked completely the relaxant effect of non-adrenergic, non-cholinergic (NANC) nerve stimulation in these tissues. 3. BRL 34915 in doses causing maximum relaxation did not increase the levels of either cyclic AMP or cyclic GMP in the BRP, although the appropriate enzymes were present and could be stimulated by forskolin or sodium nitroprusside. 4. In the BRP isoprenaline 30 microM acting through beta-receptors caused maximum relaxation but did not raise the levels of cyclic AMP, even though lower doses of 2 microM did raise the levels of this nucleotide in the rabbit uterus. 5. These results provide some indirect evidence that membrane hyperpolarization may not be the only cause of the smooth muscle relaxation induced by BRL 34915. However, neither a rise in cyclic AMP nor cyclic GMP are satisfactory alternative mechanisms.

Animals↗
PubMed1997

Minor components with smooth muscle relaxing properties from scented myrrh (Commiphora guidotti).

All sesquiterpenes present in a sample of scented myrrh were isolated and characterised. Seven compounds, with cadinane, guaiane, oplopane, and eudesmane skeletons, were obtained, of which two are new and two are reported from a natural source for the first time. The major component, T-cadinol, has previously been shown to possess smooth muscle-relaxing properties, and the major purpose of the investigation was to compare the effects of the minor and more polar sesquiterpenes with that of T-cadinol in the rat aorta. Like T-cadinol, the minor sesquiterpenes are more efficient in reducing K(+)-induced contractions than those induced by the alpha-adrenoceptor agonist phenylephrine, however, they were all less potent than T-cadinol.

Animals↗
PubMed1984

Cross-bridge attachment in relaxed muscle.

We have measured the stiffness of relaxed, skinned rabbit psoas fibers at 5 degrees C in low ionic strength relaxing solution (mu = 0.02 M) by stretching the fibers and measuring the resulting force and sarcomere length changes. This stiffness is very dependent upon the velocity of stretch. With very slow stretches (0.5% of fiber length in greater than 30 ms), it is almost negligible but with stretches as fast as 0.5% of fiber length in 150 microseconds, the stiffness approaches 1/3 that of the rigor fiber. This stiffness is also very sensitive to ionic strength, being reduced more than 20-fold at an ionic strength of 0.17 M. This ionic strength sensitive stiffness scales with the amount of overlap between the actin and myosin filaments which strongly suggests that it is due to attached cross-bridges. The speed dependence suggests that the attached cross-bridges are not statically attached but in rapid equilibrium between attached and detached states. Experiments with adenylyl-imido-diphosphate suggest that the rates of attachment and detachment depend upon nucleotide.

Adenosine Triphosphate↗
PubMed2001

Mechanism of internal anal sphincter smooth muscle relaxation by phorbol 12,13-dibutyrate.

We investigated the mechanism of the inhibitory action of phorbol 12,13-dibutyrate (PDBu), one of the typical protein kinase C (PKC) activators, in in vitro smooth muscle strips and in isolated smooth muscle cells of the opossum internal anal sphincter (IAS). The inhibitory action of PDBu on IAS smooth muscle (observed in the presence of guanethidine + atropine) was partly attenuated by tetrodotoxin, suggesting that a part of the inhibitory action of PDBu is via the nonadrenergic, noncholinergic neurons. A major part of the action of PDBu in IAS smooth muscle was, however, via its direct action at the smooth muscle cells, accompanied by a decrease in free intracellular Ca(2+) concentration ([Ca(2+)](i)) and inhibition of PKC translocation. PDBu-induced IAS smooth muscle relaxation was unaffected by agents that block Ca(2+) mobilization and Na+-K+-ATPase. The PDBu-induced fall in basal IAS smooth muscle tone and [Ca(2+)](i) resembled that induced by the Ca(2+) channel blocker nifedipine and were reversed specifically by the Ca(2+) channel activator BAY K 8644. We speculate that a major component of the relaxant action of PDBu in IAS smooth muscle is caused by the inhibition of Ca(2+) influx and of PKC translocation to the membrane. The specific role of PKC downregulation and other factors in the phorbol ester-mediated fall in basal IAS smooth muscle tone remain to be determined.

Anal Canal↗
PubMed2001

Which treatment for low back pain? A factorial randomised controlled trial comparing intravenous analgesics with oral analgesics in the emergency department and a centrally acting muscle relaxant with placebo over three days [ISRCTN09719705].

BACKGROUND: About two thirds of adults suffer from backpain at some time during their life. In the emergency room many patients with acute back pain are treated with intravenous non-steroidal analgesics. Whether this treatment is superior to oral administration of non-steroidal analgesics is unknown. Intravenous administration, however, requires considerable amounts of resources and accounts for high workload in busy clinics. In the further course centrally acting muscle relaxants are prescribed but the effectiveness remains unclear. The objective of this study is on the one hand to compare the effectiveness of intravenous with oral non-steroidal analgesics for acute treatment and on the other hand to compare the effectiveness of a centrally active muscle relaxant with placebo given for three days after presentation to the ED (emergency department). METHODS/DESIGN: This study is intended as a randomised controlled factorial trial mainly for two reasons: (1) the sequence of treatments resembles the actual proceedings in every-day clinical practice, which is important for the generalisability of the results and (2) this design allows to take interactions between the two sequential treatment strategies into account. There is a patient preference arm included because patients preference is an important issue providing valuable information: (1) it allows to assess the interaction between desired treatment and outcome, (2) results can be extrapolated to a wider group while (3) conserving the advantages of a fully randomised controlled trial. CONCLUSION: We hope to shed more light on the effectiveness of treatment modalities available for acute low back pain.

Journal Article↗
PubMed1998

Histamine receptor-independent muscle relaxation elicited by a series of histamine H2-receptor agonists on the isolated guinea pig duodenum: a study into the mechanism of action.

1. The histamine H2 receptor agonists, dimaprit, impromidine, amthamine, and several dimaprit- and impromidine-analogues were investigated for their spasmolytic activity on the guinea pig duodenum, precontracted with acetylcholine or KCl. 2. Almost all the H2 receptor agonists exerted a histamine H2 receptor-independent muscle relaxation, which was more evident on acetylcholine- than on KCl-precontracted preparations. 3. The relaxing activity of these compounds was independent of inhibitory receptors, like beta-adrenergic, GABA-ergic, serotoninergic, etc. Similarly, modifications of cyclic nucleotide metabolism and nitric oxide production did not appear to be involved. 4. The behavior of histamine H2-receptor agonists was shared only by the Na+-blocker procaine, the intracellular Ca2+-antagonist ruthenium red and, at least in terms of efficacy, by the protein kinase C inhibitor, chelerithrine. 5. This spasmolytic effect is probably due to an impairment of receptor-mediated depolarization at the plasma membrane level and/or an inhibitory activity on the protein kinase C-dependent activation of the contractile machinery. 6. Finally, our findings suggest that the histamine H2 receptor-independent muscle relaxation is a general feature shown by H2 receptor agonists endowed with different chemical structure and the putative spasmolytic "receptor" prefers a (substituted) thiazole over a (substituted) imidazole.

Animals↗
PubMed1992

Desensitization of beta-adrenoceptor- and prostaglandin E1 receptor-mediated human vascular smooth muscle relaxation.

Regulation of beta-adrenoceptors in animal tissues and human cell cultures has been extensively described; on the other hand, relatively little is known about regulation of beta-adrenoceptors in human tissues in vivo. Both beta-adrenoceptors and the prostaglandin E1 (PGE1) receptors stimulate vasodilation. We wondered if prolonged infusion of isoproterenol or PGE1 would cause desensitization of smooth muscle relaxation and used the dorsal hand-vein compliance technique to investigate this question. After constructing a dose-response curve to either the beta-agonist isoproterenol or to PGE1 in a phenylephrine preconstricted vein, isoproterenol (271 ng/min), PGE1 (956 pg/min), or saline was infused for 4 h in separate experiments. There was no change in the ED50 or Emax for either isoproterenol or PGE1 after saline infusion. After a 4-h infusion of isoproterenol, the maximal vasodilator response to isoproterenol was significantly (p less than 0.01) attenuated from 61 +/- 33% to 19 +/- 10%, while the ED50 significantly increased (p less than 0.01) from a geometric mean of 37 to 197 ng/min. After infusion of isoproterenol, the mean maximum PGE1-induced venorelaxation of 129 +/- 29% was modestly but significantly (p less than 0.05) blunted to 96 +/- 35%, while the ED50 of PGE1 increased significantly (p less than 0.01) from a geometric mean of 81 to 398 pg/min. A 4-h infusion of PGE1 significantly (p less than 0.01) attenuated the maximum response to PGE1 from 73 +/- 35 to 28 +/- 16%. The maximal vasodilatory response to isoproterenol was also significantly blunted (p less than 0.05) from 62 +/- 35 to 42 +/- 41%, with no change in ED50.(ABSTRACT TRUNCATED AT 250 WORDS)

Alprostadil↗
PubMed1989

[Interactions of H2 antagonists and non-depolarizing muscle relaxants].

Many drugs potentiate the action of non depolarizing relaxants. These interactions are of clinical importance if such drugs are administered during the perioperative period. H2 Antagonists are increasingly often used for premedication. Cimetidine inhibits the elimination of a number of drugs used in the perioperative period. We therefore investigated whether H2 antagonists enhanced neuromuscular blockade by vecuronium, a medium short acting non depolarizing muscle relaxant. METHODS. The study was carried out in 24 female patients (ASA class I or II) scheduled for microsurgical procedures. Neuromuscular transmission was recorded electromyographically using four stimulations every 20 s to the ulnar nerve. After induction with thiopentone, anesthesia was maintained with fixed concentrations of volatile anesthetics. Fentanyl was administered for additional analgesia. Vecuronium was used as the sole muscle relaxant. Fixed repetitive doses of vecuronium (0.8-1.2 mg) were injected whenever the T1 returned to 25%. This time interval was defined as the T1-25 period. The study proper started when the T1-25 period had stabilized. After two control periods, six patients in each group received either 200 or 400 mg cimetidine or 100 mg ranitidine. The fourth group was the control group. The T1-25 periods and the maximal EMG depression were recorded automatically for at least two further periods. The first measured period was recorded as 100% and the length of each other periods was calculated as a percentage of the control period. This method enables an intraindividual comparison of the length of the T1-25 period and the maximal EMG depression before and after administration of the H2 antagonists. A two-tailed Student's t-test was used to test statistical significance, P less than 0.05 being accepted as significant. RESULTS. In the control group and in the group with 200 mg cimetidine or 100 mg ranitidine no statistical significant prolongation of the T1-25 period or of the maximal EMG depression could be observed, while after 400 mg cimetidine there was significant prolongation (mean 161 +/- 14.8%) of the T1-25 period and significantly greater EMG depression compared with the pre-cimetidine values. In the groups with 200 mg cimetidine or 100 mg ranitidine few patients showed prolongation of the T1-25 period up to 130%. DISCUSSION. Our results confirm experimental studies that have shown cimetidine to enhance aminoglycoside--relaxant interactions. Because we found an immediate response to the administration of the H2 antagonists, the interaction cannot be on the elimination side; it must be at the neuromuscular junction. Experimental investigation has shown that calcium reverses the cimetidine effects. It is therefore probable that the cimetidine--relaxant interaction occurs at the presynaptic level. Careful observation seems to be necessary if H2 antagonists, especially cimetidine, are administered intraoperatively at the same time as drugs that also enhance

Adult↗
PubMed1981

Correlation between vascular smooth muscle relaxation and increase in cyclic GMP induced by some organic nitro esters.

Three different nitro compounds glyceryl mononitrate (GMN), glyceryl dinitrate (GDN) and ethylene glycol dinitrate (EGDN) were tested on histamine contracted bovine mesenteric artery. GDN and EGDN caused a dose-dependent relaxation which was accompanied by an increase in the endogenous cGMP level. The ED50-value for GDN and EGDN with regard to the relaxant action was 1.06 X 10(-6) M and 4.20 X 10(-8), respectively. GMN was almost completely ineffective as a relaxing agent and did not cause any significant change in cGMP. Regression analysis revealed a significant correlation between relaxation and increase in cGMP for both GDN and EGDN. The regression model for EGDN could be significantly improved by including the squared cGMP change, indicating a non-linear relationship. With regard to GDN a hyperbolic relationship between relaxation and cGMP increase was found. A slight improvement of the regression model was found for EGDN when the change in cAMP was included. For GMN and GDN no improvement of the regression model could be revealed by including the change of cAMP. It is suggested that the present data give further evidence for cGMP as a mediator of vascular smooth muscle relaxation induced by nitro compounds.

Animals↗
PubMed1978

Identification of hydrallazine and hydrallazine hydrazone metabolites in human body fluids and quantitative in vitro comparisons of their smooth muscle relaxant activity.

1 Serum and urine from hypertensive subjects on chronic oral hydrallazine therapy were studied using gas chromatographic/mass spectrometry techniques. 2 Metabolites resulting from acetylation, hydrolysis and conjugation reactions were detected. The acetone, pyruvate and alpha-ketoglutarate hydrazone were identified. 3 The activity of the pyruvate and alpha-ketoglutarate hydrazones were compared with that of hydrallazine using isolated rabbit aortic strips. 4 Both hydrazones were active under in vitro conditions, producing smooth muscle relaxant effects equal to those of hydrallazine. 5 It is concluded that hydrazone metabolites will contribute to the hypotensive effects of hydrallazine therapy in proportion to their relative abundance, persistence in vascular tissues and intrinsic activity.

Animals↗
PubMed1982

Mechanism of action of dantrolene sodium, a peripherally acting muscle relaxant.

The mechanism of action of dantrolene sodium, a peripherally acting muscle relaxant, is reviewed. It does not alter action potentials or responses of the contractile proteins to Ca. The amount of Ca acting on the contractile proteins during twitch must, therefore, be reduced, but since Ca uptake by the SR is not altered, Ca release from the SR must be reduced by the drug. Other characteristics of this drug and their clinical implications are discussed.

Action Potentials↗
PubMed1963

[Muscle relaxants].

Explore the source record for details and available documents.

Cardiovascular Agents↗
PubMedDate not supplied

Muscle-relaxant activity in Asian Strychnos species. A re-examination of two western Malaysian dart poisons.

Two supposedly Strychnos-based Semai Senoi dart poisons from Western Malaysia, ipoh akar and lampong, and their accompanying plant materials have been re-investigated botanically, chemically, and pharmacologically. The two poisons contained tertiary and quaternary alkaloids, including strychnine and bis-quaternary dimeric bases, and also cardiotonic glycosides. The dominant pharmacological activity of the highly toxic ipoh akar poison was convulsant. The weaker lampong poison had muscle-relaxant activity of the curarizing type. The alkaloids of the two poisons were almost certainly derived from Strychnosignatii Berg. (S. ovalifolia Wall. ex G. Don) and not from S. vanprukii Craib to which the accompanying plant materials probably belong, while the cardiotonic glycosides of the two poisons came from Antiaris toxicaria Lesch. The quaternary alkaloids of both S. ignatii and S. vanprukii have muscle relaxant activity.

Alkaloids↗
PubMed1979

Effects of muscle relaxants on catecholamine release from adrenal medulla.

Bovine adrenals were perfused with secretagogues in the presence or absence of muscle relaxants. On a molar basis, Dially-nor-toxiferine was as potent as tubocurarine in inhibiting the catecholamine release induced by carbachol; pancuronium was about 100 times less potent than tubocurarine, whereas gallamine and succinylcholine produced no inhibition whatsoever. KCl-induced catechoamine release was not affected by any of these compounds. Nicotine-induced catecholamine release was inhibitedby diallyl-nor-toxiferine, tubocurarine and pancuronium, but not by gallamine or succinylcholine. Muscarine failed to stimulate the adrenal medulla to release catecholamines. The results show that the inhibition of catecholamine release is based on the specific block of the nicotinic receptor, whereas gallamine and succinylcholine possess no blocking action, and that diallyl-nor-toxiferine and tubocurarine might affect clinical symptoms under conditions in which catecholamine release from the adrenal is increased by a compensatory mechanism.

Adrenal Medulla↗