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At least 19 recordsLinked to original sources
PubMed1963

The nature of the muscle-relaxing factor. II. Some physicochemical properties.

High speed centrifugal fractionation of homogenates of rabbit skeletal muscle has led to the discovery of a soluble muscle-relaxing factor in the homogenate. Assay of the relaxing activity with deoxycholate-treated myofibrils and reconstituted actomyosin systems has established that the activity is not produced by the presence of contaminants. Relaxing activity could be removed or destroyed by charcoal, dialysis, prolonged heating, and treatment with the chelating resin, chelex-100, making it improbable that the effect is due simply to calcium deficiency. Many of the characteristics of this muscle-relaxing factor suggest that it is very similar to or the same as the factor formed by the incubation of muscle granule fractions and ATP. Evidence is presented that some soluble protein component is involved in the stabilization of the factor. The relaxing activity could be separated from the high molecular weight material in the supernatant by the technique of gel filtration. On the basis of the gel used, the molecular weight of the active agent should be less than 4000.

Actomyosin↗
PubMed1963

The nature of the muscle-relaxing factor. I. An improved assay system.

Analysis of the effects of deoxycholate and benzalkonium chloride on granule relaxing activity, myofibril and glycerinated fiber responses to ATP, and the sensitivity of these actomyosin-containing systems to relaxing factors have established that it is possible to differentially inactivate intrinsic granule relaxing factor. It is therefore possible to use these agents to treat myofibrils and glycerinated muscle fibers so that they may be used for the assay of muscle-relaxing factor preparations. The destruction of intrinsic relaxing factor can be produced by treating actomyosin with 1 mM deoxycholate or 0.005 per cent benzalkonium chloride for 5 minutes at room temperature.

Actomyosin↗
PubMed1986

Tracheal epithelium releases a vascular smooth muscle relaxant factor: demonstration by bioassay.

Acetylcholine caused no relaxation of a rubbed strip from rabbit aorta (RASR) which was precontracted with phenylephrine. When the same strip was taken into epithelium-intact guinea-pig trachea, acetylcholine produced a slow-developing relaxation which was antagonized by atropine but not by propranolol, indomethacin, theophylline or hydroquinone. RASR was not relaxed by acetylcholine when it was taken from epithelium-rubbed trachea. The results indicate that acetylcholine releases vascular smooth muscle relaxant factor from tracheal epithelium.

Acetylcholine↗
PubMed1994

Induction of muscle-relaxing factor by staphylococcal alpha-toxin.

Brain tissue and serum from mice intracerebrally injected with 1 microgram of staphylococcal alpha-toxin contained elevated amounts of a naturally occurring brain tissue component(s) called muscle-relaxing factor (MRF). MRF induced reversible, generalized, flaccid paralysis of mice after intracerebral but not intraperitoneal or intravenous administration. MRF (i) was soluble in Hanks balanced salt solution and in acidified (pH 2) Hanks balanced salt solution, in which it partitions into ethyl acetate, acetone, and methanol; (ii) was separated from some pigments by thin-layer chromatography on silica gel plates; (iii) did not comigrate with prostaglandin and leukotriene standards during high-pressure liquid chromatography with a mu Bondapak fatty acid column; and (iv) did not contain amino acids, exhibit absorption maxima at a wavelength range of 210 to 600 nm, or fluoresce when exposed to UV light. MRF has been detected in rabbit brain that has been stored frozen at -70 degrees C and has been enhanced in vitro in slices of both mouse and rabbit brain following incubation of the brain slices with staphylococcal alpha-toxin. Studies to identify the chemical nature of MRF and the mechanism by which, in mice, it induces reversible, flaccid paralysis of voluntary muscle are continuing.

Animals↗
PubMed1989

Co-axial bioassay of a smooth muscle relaxant factor released from guinea-pig tracheal epithelium.

1. The ability of guinea-pig trachea to release an epithelium-derived relaxant factor (EpDRF) was assessed in a co-axial bioassay system. 2. Histamine (100 microM) and methacholine (25 microM) caused endothelium-dependent relaxation of rat isolated aorta, presumably via the release of endothelium-derived relaxant factor (EDRF). In contrast, endothelium-denuded rat aorta did not relax in response to these agents. 3. EDRF release was detected in response to methacholine in a co-axial bioassay system, consisting of intact rabbit aorta tube (EDRF donor) and endothelium-denuded rat aorta strip (assay preparation). These results indicated the transfer of EDRF from a donor to an assay preparation, thereby validating the co-axial bioassay method. 4. Substitution of endothelium-intact rabbit aorta tube by epithelium-intact guinea-pig tracheal tube tissue in co-axial assemblies, still allowed the assay preparation to relax in response to histamine or methacholine. Removal of the intact tracheal tube from the system, or removal of the epithelium from the donor tracheal tube in co-axial preparations, abolished such relaxant responses. These observations are consistent with histamine- or methacholine-induced release of an epithelium-derived relaxant factor (EpDRF) from the trachea. 5. In the co-axial assembly comprising intact guinea-pig trachea and endothelium-denuded rat aorta, histamine and methacholine produced concentration-dependent, EpDRF-induced aortic relaxation. Mean concentrations of histamine and methacholine producing 50% of the maximum relaxation (EC50) were 39.8 microM and 2.7 microM respectively. Histamine-induced relaxation was inhibited in the presence of mepyramine (2 microM) and responses to methacholine were inhibited by atropine (0.1 microM). 6. Methylene blue (50 microM) had no effect on such relaxant responses, indicating that EpDRF does not activate guanylate cyclase. Furthermore, the cyclo-oxygenase inhibitor indomethacin (5 microM), the cyclo-oxygenase/lipoxygenase inhibitor BW 755C (150 microM) and the leukotriene receptor antagonist FPL 55712 (10 microM) each failed significantly to alter EpDRF-mediated relaxation of vascular smooth muscle suggesting that EpDRF is not a prostanoid. Platelet activating factor (Pat) failed to cause relaxation of endothelium-denuded rat aorta, indicating that this mediator was also not EpDRF. 7. EpDRF was also released from human bronchial segments. 8. This study provides direct evidence for the release of an EpDRF from non-diseased airway tissue and further suggests that healthy airway reactivity to spasmogens is modulated by the release of an endogenous protective, spasmolytic substance. The bronchial hyperreactivity of asthma may be partly caused by attenuated production of such an inhibitory signal.

Animals↗
PubMed1999

A non-nitrergic smooth muscle relaxant factor released from rat urinary bladder by muscarinic receptor stimulation.

PURPOSE: To study the possible release of a relaxant factor from isolated rat bladder tissue. MATERIALS AND METHODS: Thoracic aortae and urinary bladders were obtained from 55 female Sprague-Dawley rats. The bladder body was used in its original tubular shape as the donor tissue in a co-axial bioassay system, and the aorta served as acceptor tissue. RESULTS: In a co-axial bioassay system with endothelium-free, norepinephrine-contracted, rat aortic preparations mounted within urothelium-intact urinary bladder, carbachol caused a concentration-dependent relaxation, amounting to 64+/-7% (n = 10) of the induced contraction, suggesting release of a relaxing factor. The relaxant effect of carbachol was lost if the urinary bladder segment was removed. However, the relaxation was affected neither by removal of the urothelium, nor by bladder segment inversion. It was resistant to inhibition of the L-arginine/nitric oxide and cyclo-oxygenase pathways, and unaffected by beta-adrenoceptor blockade and K+ channel inhibition. The relaxation was not associated with any significant changes in the intracellular levels of cGMP or cAMP. CONCLUSION: A previously unrecognized non-adrenergic, non-nitrergic, non-prostanoid inhibitory mediator is released from the rat urinary bladder by muscarinic receptor stimulation. The physiological importance of such a factor remains to be established.

Animals↗
PubMed1987

A relaxing factor released by phospholipase A2 in the absence of endothelium.

Phospholipase A2 (PLA2) produced slow dose dependent relaxation in intact and endothelium-deprived precontracted rabbit aortic strips. In endothelium-deprived preparations, relaxation induced by PLA2 is inhibited by hemoglobin, methylene blue and parabromophenacylbromide (PBPB), and is potentiated by superoxide dismutase (SOD). Indomethacin has no effect. Relaxation is accompanied by a rise in c-GMP. Phospholipase C causes a significant increase in tension, while Phospholipase D has no effects. In intact aortic strips PLA2 causes a biphasic response with no elevation in c-GMP. The results indicate several common features of the PLA2 released factor with endothelium-derived relaxing factor (EDRF). However, PLA2 induced relaxation is not dependent on endothelial cells. Apparently in addition to nitric oxide which may be the endothelium-derived relaxing factor, a second smooth muscle relaxing factor exists which is initiated by PLA2 and is independent of endothelium. The production of the PLA2 produced relaxation is dependent on its specific hydrolytic activity. We call this relaxing factor the phospholipid-derived relaxing factor (PDRF).

Animals↗
PubMed1990

Vascular smooth muscle-derived relaxing factor (MDRF) and its close similarity to nitric oxide.

The principal finding in this study is that vascular smooth muscle generates a labile relaxing factor that possesses pharmacological and chemical properties that are similar to those of authentic nitric oxide. MDRF was generated by perfusion of endothelium-denuded bovine pulmonary artery as assessed by bioassay. In addition, endothelium-denuded arterial rings that were incubated at 37 degrees C for 24 hr to lower endogenous L-arginine levels relaxed in response to L-arginine but not D-arginine. Freshly mounted, endothelium-denuded arterial rings were not relaxed by L-arginine but did relax in response to the dipeptide L-arginyl-L-alanine. Relaxant responses were accompanied by increases in smooth muscle levels of cyclic GMP and nitrite, and were inhibited by oxyhemoglobin, methylene blue, and NG-nitro-L-arginine. NG-Nitro-L-arginine also caused endothelium-independent contractile responses. Thus, a relaxing factor with the properties of nitric oxide can be generated from vascular smooth muscle.

Animals↗