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Results for “Muscle Relaxation”

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At least 1,747 records · Page 97Linked to original sources
PubMed1988

Pharmacological evidence that endothelium-derived relaxing factor is nitric oxide: use of pyrogallol and superoxide dismutase to study endothelium-dependent and nitric oxide-elicited vascular smooth muscle relaxation.

The principal objective of this study was to elucidate the influence of superoxide anion on both endothelium-dependent arterial relaxation elicited by acetylcholine and endothelium-independent arterial relaxation produced by nitric oxide (NO). Pyrogallol was used to generate superoxide in the oxygenated bathing medium, and superoxide dismutase was used to scavenge superoxide. Pyrogallol caused endothelium-dependent contractions of bovine intrapulmonary arterial and venous smooth muscle after precontraction of muscle by phenylephrine. Acetylcholine- and NO-elicited arterial relaxations were promptly converted to marked contractions upon addition of pyrogallol. Moreover, pyrogallol markedly inhibited the development of arterial relaxant responses to acetylcholine and NO. However, isoproterenol- and glyceryl trinitrate-elicited arterial relaxations were unaffected by pyrogallol. Both pyrogallol and oxyhemoglobin enhanced arterial contractile responsiveness to phenylephrine in an endothelium-dependent manner, whereas indomethacin was without effect. Similarly, both pyrogallol and oxyhemoglobin inhibited acetylcholine- and NO-elicited arterial cyclic GMP accumulation, whereas indomethacin was without effect. Uncontracted arterial rings maintained under tension showed endothelium-dependent contraction and decreased cyclic GMP levels in response to oxyhemoglobin but not pyrogallol. Superoxide dismutase enhanced arterial relaxation and cyclic GMP accumulation in response to both acetylcholine and NO. Using a bioassay superfusion cascade system in which intact perfused artery was the source of endothelium-derived relaxing factor (EDRF) and three endothelium-denuded arterial strips mounted in series served as the detector of EDRF, superfusion of strips with pyrogallol blocked relaxation caused by perfusion of artery with acetylcholine. Superoxide dismutase enhance the relaxations produced by arterial perfusion with acetylcholine and prevented the effects of pyrogallol.

Animals↗
PubMed1990

Beta 1-adrenoceptors mediate smooth muscle relaxation in mouse isolated trachea.

1. The relaxant effects to the beta-adrenoceptor agonists isoprenaline, adrenaline, noradrenaline, RO363, procaterol and fenoterol were investigated in carbachol-contracted mouse isolated tracheal preparations. 2. The order of potencies for those beta-adrenoceptor agonists that induced full relaxation of carbachol-contracted mouse tracheal preparations was isoprenaline greater than RO363 greater than noradrenaline = adrenaline greater than fenoterol. The EC50 value of isoprenaline for relaxation was 46 nM. The beta 1-adrenoceptor-selective agonist, RO363 was ten times more potent than the beta 2-adrenoceptor-selective agonist, fenoterol. The highly beta 2-adrenoceptor-selective agonist procaterol was a partial relaxant and induced only 28 +/- 4% relaxation. 3. Relaxations induced by noradrenaline and isoprenaline were not significantly affected by the neuronal uptake inhibitor, cocaine (10 microM) or by the extraneuronal uptake inhibitor, deoxycorticosterone acetate (25 microM) respectively. The alpha-adrenoceptor agonist methoxamine induced no observable elevation of mouse tracheal smooth muscle tone. 4. Schild plots for the beta-adrenoceptor antagonists, atenolol and betaxolol (beta 1-adrenoceptor-selective) and ICI 118,551 (beta 2-adrenoceptor-selective) were linear, with slope values approaching unity. Mean pA2 values derived for atenolol, betaxolol and ICI 118,551 for antagonism of beta-adrenoceptor-mediated relaxation were 7.1, 8.4 and 7.2, respectively. These data were independent of the use of isoprenaline or noradrenaline as the agonist. 5. These findings indicate that beta-adrenoceptor-mediated relaxations of mouse isolated trachea occur predominantly through activation of beta 1-adrenoceptors.

Animals↗
PubMed1987

Mechanisms of endothelium-dependent vascular smooth muscle relaxation elicited by bradykinin and VIP.

The objective of this study was to elucidate the mechanisms by which bradykinin and vasoactive intestinal polypeptide (VIP) relax bovine intrapulmonary artery and bradykinin, but not VIP, relaxes intrapulmonary vein. Bradykinin and VIP elicited entirely endothelium-dependent relaxation of phenylephrine-precontracted arterial rings, and this was associated with arterial accumulation of both guanosine 3',5'-cyclic monophosphate (cGMP) and adenosine 3',5'-cyclic monophosphate (cAMP). Bradykinin, but not VIP, relaxed precontracted venous rings and increased cGMP, but not cAMP levels, by endothelium-dependent mechanisms. Neither arteries nor veins relaxed in response to substance P, thrombin, bombesin, arginine vasopressin, or angiotensin II. Methylene blue or indomethacin each partially antagonized, whereas both, when together, abolished arterial relaxant responses to bradykinin and VIP. Methylene blue or indomethacin, respectively, abolished arterial cGMP or cAMP accumulation elicited by bradykinin and VIP. Venous relaxation and cGMP accumulation elicited by bradykinin was abolished by methylene blue but was unaltered by indomethacin. Thus bradykinin and VIP relaxed bovine intrapulmonary artery by endothelium-dependent mechanisms involving the actions of cGMP and cAMP whose formation may be stimulated by endothelium-derived relaxing factor and prostacyclin, respectively. In contrast, bradykinin relaxed intrapulmonary vein by endothelium-dependent mechanisms involving only cGMP.

Animals↗
PubMedDate not supplied

[The presynaptic action of muscle relaxants and cholinesterase inhibitors].

This is a review of literature dealing with the action of relaxants and cholinesterase inhibitors on the skeletal muscles. They act on the presynaptic motor nerve endings in the muscles and, depending on the experimental conditions, increase or inhibit the release of acetylcholine by the endings. According to the literature data, two types of acetylcholine receptors (AchR) exist on the endings of a motor nerve. The neuronal type of AchR is related to a negative feedback mechanism and their blockade increases the release of acetylcholine by the motor nerve ending. Blockade of the muscular-type AchR is related to a positive, feedback mechanism and inhibits the release of acetylcholine.

Acetylcholine↗
PubMed1983

[Use of muscle relaxation in the primary prevention of ischemic heart disease].

Possibilities of using muscular relaxation as a general hygienic procedure that helps reducing the risk of coronary disease were examined in males and females from an open random population at preventive group sessions. Their ability to learn the techniques of muscular relaxation and the effects of relaxation on arterial pressure were assessed. A course of four group sessions completed by 23.23% of volunteers was sufficient for 86.36% of males and 91.49% of females to learn the command of muscular relaxation. Arterial pressure decreased significantly between the beginning of the first session and the last one (p less than 0.01), the lowered level persisting at the control session in three months' time (p less than 0.01). Muscular relaxation is expected to provide a useful element of preventive population programs aimed at reducing moderately elevated arterial pressure.

Adult↗
PubMed1991

Species differences and the role of sodium-calcium exchange in cardiac muscle relaxation.

During normal relaxation in rabbit, guinea-pig, and rat ventricular muscle, the Na-Ca exchange system competes with the SR Ca pump, with the former being responsible for about 20-30% of the Ca removal from the cytoplasm. Ca extrusion via Na-Ca exchange is Em-sensitive, whereas Ca uptake by the SR is not. Neither the sarcolemmal Ca-ATPase pump nor mitochondrial Ca uptake appear to contribute significantly to the decline of [Ca]i during relaxation. Furthermore, the diastolic efflux of Ca from cardiac muscle cells appears to be primarily attributable to Na-Ca exchange and not the sarcolemmal Ca-ATPase pump. In rabbit ventricle Ca entry via Na-Ca exchange is favored thermodynamically during much of a normal twitch contraction and Ca extrusion occurs primarily between beats. In rat ventricle Ca efflux via Na-Ca exchange occurs during the contraction and net Ca influx may occur between beats. This fundamental difference in Ca fluxes during the cardiac cycle in rat versus rabbit ventricle may be a simple consequence of the shorter action potential duration and higher aNai in rat ventricle (due to the effects of Em and [Na] and [Ca] gradients on Na-Ca exchange).

Animals↗
PubMed1987

Comparison of the skeletal muscle relaxant properties of Portulaca oleracea extracts with dantrolene sodium and methoxyverapamil.

The effects of aqueous (AEE), dialysable (DIF) and methanol (MEE) extracts of Portulaca oleracea stems and leaves were compared with those of dantrolene sodium and methoxyverapamil (D-600) with respect to inhibition of twitch tension on the rat phrenic nerve-hemidiaphragm and with respect to contracture induced by nicotinic agonists on the frog rectus abdominis preparations. The extracts, dantrolene and D-600 inhibited twitch tension due to indirect electrical stimulation via the phrenic nerve (NS) on hemidiaphragm muscle, whereas the extracts and dantrolene inhibited, in addition, twitch amplitude due to direct muscle stimulation (MS). The extracts, dantrolene and D-600 also attenuated K+- and caffeine-induced contractures with the extracts and D-600 also reducing the time taken for the K+-induced contracture to fall to basal tension. In addition, the tetanic tension due to NS and MS was attenuated with only the extracts and dantrolene reducing the twitch/tetanus ratio (MS). There was a non-significant but consistent tendency for mutual potentiation between the extracts and dantrolene with respect to their inhibitory effect on twitch amplitude (MS) resulting in a shift to the left of the concentration-response curves to the extracts or dantrolene. This was not evident with the extracts and D-600 or dantrolene and D-600. Simultaneous addition of the extracts and dantrolene resulted in an increase in the rate of twitch tension inhibition and a decrease in the time to maximum relaxation of twitch amplitude (MS). The extracts and D-600 proved more effective in attenuating nicotinic agonist (acetylcholine, carbachol and nicotine)-induced contractures on the rectus abdominis muscle than dantrolene. From these observations, it appears that the Portulaca oleracea extracts mimic, in part, the effect of D-600 and dantrolene on the rat hemidiaphragm and frog rectus abdominis muscles; therefore, the muscle relaxant properties of the extracts may be due, in part, to inhibition of trans-membrane Ca influx, interference with the Ca-induced Ca release process and/or inhibition of the release of intracellular Ca from stores in the sarcoplasmic reticulum.

Animals↗