Muscle inhibition

Somlyo What is Gd3+ doing to I. type channels, and what if arachidonic acid in smooth muscle inhibits L-type channels ... 

Paralyzes helminth muscle Inhibits production of energy... 

Alpha2 Presynaptic adrenergic nerve terminals, platelets, lipocytes, smooth muscle Inhibition of adenylyl cyclase, decreased cAMP... 

The best-characterized action of the adrenoceptor agonists in the airways is relaxation of airway smooth muscle. Although there is no evidence for direct sympathetic innervation of human airway smooth muscle, ample evidence exists for the presence of adrenoceptors on airway smooth muscle. In general, stimulation of 32 receptors relaxes airway smooth muscle, inhibits mediator release, and causes tachycardia and skeletal muscle tremor as adverse effects. 

Opioids induce an inhibitory effect on gastrointestinal motility and fluid secretion (Kromer, 1990). The effect is peripherally and centrally mediated. The peripheral component is related to p- and K-receptors in intestinal organs, which are densely equipped with opioid receptors. They are located at parasympathic ganglia and inhibit the release of acetylcholine, which stimulates the contraction of smooth muscles. Inhibition of the intestinal fluid secretion is mediated via inhibition of adenylate cyclase. The intestinal effects of opioids extend to all parts of the gut and results in inhibition of stomach emptying and inhibition of secretion and motility of duodenum, jejunum, colon and rectum. 

Muller, F., Heath, M.R., Kazazoglu, E. and Hector, M.P. (1993). Contribution of periodontal receptors and food quality to masseter muscle inhibition in man. J. Oral Rehab. 20, 281-290. 

The bipyridines increase myocardial contractility by increasing inward calcium flux in the heart during the action potential they may also alter the intracellular movements of calcium by influencing the sarcoplasmic reticulum. They also have an important vasodilating effect. These drugs are relatively selective for phosphodiesterase isozyme 3, a form found in cardiac and smooth muscle. Inhibition of this isozyme results in an increase in cAMP and the increase in contractility and vasodilation noted above. 

BoNTs are a group of immunologically distinct but closely related bacterial proteins that act as potent inhibitors of synaptic transmission in skeletal muscle. Inhibition of ACh release from the presynaptic terminal of the neuromuscular junction (NMJ) is thought to be the sole mechanism involved in the toxins lethal action (Sellin, 1985 Simpson, 1986) and therefore the cause of botulism. The pathogenesis of intoxication is not completely understood but is generally thought to involve a multistep process to interrupt normal vesicular release of ACh Ifom the presynaptic motor nerve... 

Wang, M.X., Murrell, D.F., Szabo, C. et al. (2001). Nitric oxide in skeletal muscle inhibition of nitric oxide synthase inhibits walking speed in rats. Nitric Oxide Biol. Chem. 5 219-32. 

Neosaxitoxin, saxitoxin, and gongantoxin I-IV block transmission of impulses between nerve and muscle. They also block sodium channels in nerve and skeletal muscle, inhibiting the nerve and muscle action potential, thereby blocking nerve conduction and muscle contraction. 

The inhalational anesthetics halothane, isoflurane, and enflu-rane all have been reported to have a positive effect in children and adults with severe asthma that is unresponsive to standard medical therapy. The proposed mechanisms for inhalational anesthetics include direct action on bronchial smooth muscle, inhibition of airway reflexes, attenuation of histamine-induced bronchospasm, and interaction with /32-adrenergic receptors. Well-controlled trials with these agents have not been completed. Potential adverse effects include myocardial depression, vasodilation, arrhythmias, and depression of mucociliary function. In addition, the practical problem of delivery and scavenging these agents in the intensive care environment as opposed to the operating room is a concern. The use of volatile anesthetics cannot be recommended based on insufficient evidence of efficacy. 

Neuromodulator - peripheral Schistocerca Extensor -tibiae muscle Inhibits myogenic contractions Modulates neuromuscular transmission DUMETi 2 41,42... 

The stage was then set for Ahlquist s (1948) classic experiments leading to the proposal of a and 3 adrenoceptors. The research was based on sensitivities to NE and EP and related substances. In essence, he discovered an inverse potency relationship between producing excitation in smooth muscles (peripheral vasoconstriction, uterus, ureter) and intestinal smooth muscle inhibition—Set A—and the production of vascular inhibition (vasodilation) and of the uterus, and cardiac excitation—Set B. The experimentation utilized dogs, cats, and rabbits as well as isolated animal tissues. The amines tested showed a decreasing potency in the order listed for Set A effects, and the opposite for Set B effects ... 

The cardiomyopathy is directly related to a reduction in the normal biochemical function of the vitamin thiamine in heart muscle. Inhibition of the a-keto acid dehydrogenase complexes causes accumulation of a-keto acids in heart muscle (and in blood), resulting in a chemically-induced cardiomyopathy. Impairment of two other functions of thiamine may also contribute to the cardiomyopathy. Thiamine pyrophosphate serves as the coenzyme for transketolase in the pentose phosphate pathway, and pentose phosphates accumulate in thiamine deficiency. In addition, thiamine triphosphate (a different coenzyme form) may function in Na conductance channels. 

Matsuo M, Reardon S, Ikebe M, Kitazawa T (1994) A novel mechanism for the Ca -sensitizing effect of protein kinase C on vascular smooth muscle inhibition of myosin light chain phosphatase. J Gen Physiol 104 265-286 McDaniel NL, Rembold CM, Murphy RA (1994) Cyclic nucleotide dependent relaxation in vascular smooth muscle. Can J Physiol Pharmacol 72 1380-1385 Murphy RA (1994) What is special about smooth muscle The significance of covalent crossbridge regulation. FASEB J 8 311-318... 

Ferguson, W. S., Ashworth, R. de B., and Terry, R. A. 1950. Nature of a muscle-inhibiting compound in lucerne and its possible connexion with bloat in cattle. Nature 166, 116. 

Figure 3.23 Regulation of -oxidation in muscle. = Inhibition of enzymes indicated.

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