Muscle contraction inhibition

Alpha-adrenoceptor antagonists inhibit the activation of a adrenoceptors by catecholamines. In the cardiovascular system these receptors are mainly located on the surface of smooth muscle cells in the walls of arteries and veins. On activation, they mediate an increase in intracellular free calcium, which induces smooth muscle contraction. Inhibition by an a antagonist causes arterial or venous vasodilatation. The postsynaptic effect is mainly mediated by ol adrenoceptors whereas o2 adrenoceptors are found on the presynaptic membranes of the sympathetic neurones. Activation of o2-adreno-ceptors results in auto-inhibition of catecholamine release. 

Causes release of Ca from muscle storage sites this leads to muscle contraction. Inhibits return of Ca to storage sites, prolonging muscle contraction. 

Aorta endothelial Muscle contraction inhibition Rosie et al., 1991... 

Basilar artery endothelial Muscle contraction inhibition Ea Kim et al., 1990... 

Muscle contraction inhibition Djuric and Andjelkovic, 1995 Djuric et al., 1996... 

The eicosanoids produced by the cyclooxygenase reaction exert a range of profound activities at concentrations down to 10" g per gram tissue. These are now known to include effects on smooth muscle contraction, inhibition or stimulation of platelet stickiness, bronchoconstriction/dilation and vasoconstriction/dilation with a consequent influence on blood pressure. The effect on smooth muscle contraction was the earliest to be recognized and has been much used as a biological assay for eicosanoids. This use has been largely replaced by modern analytical methods such as gas... 

Phosphodiesterase Inhibitors. Because of the complexity of the biochemical processes involved in cardiac muscle contraction, investigators have looked at these pathways for other means of dmg intervention for CHF. One of the areas of investigation involves increased cycHc adenosine monophosphate [60-92-4] (cAMP) through inhibition of phosphodiesterase [9025-82-5] (PDE). This class of compounds includes amrinone, considered beneficial for CHF because of positive inotropic and vasodilator activity. The mechanism of inotropic action involves the inhibition of PDE, which in turn inhibits the intracellular hydrolysis of cAMP (130). In cascade fashion, cAMP-catalyzed phosphorylation of sarcolemmal calcium-channels follows, activating the calcium pump (131). A series of synthetic moieties including the bipyridines, amrinone and milrinone, piroximone and enoximone, [77671-31-9], C22H22N2O2S, all of which have been shown to improve cardiac contractiUty in short-term studies, were developed (132,133). These dmgs... 

The action of epinephrine and related agents forms the basis of therapeutic control of smooth muscle contraction. Breathing disorders, including asthma and various allergies, can result from excessive contraction of bronchial smooth muscle tissue. Treatment with epinephrine, whether by tablets or aerosol inhalation, inhibits MLCK and relaxes bronchial muscle tissue. More specific bronchodilators, such as albuterol (see figure), act more selec-... 

Ca2+ is an important intracellular second messenger that controls cellular functions including muscle contraction in smooth and cardiac muscle. Ca2+ channel blockers inhibit depolarization-induced Ca2+ entry into muscle cells in the cardiovascular system causing a decrease in blood pressure, decreased cardiac contractility, and antiarrhythmic effects. Therefore, these drugs are used clinically to treat hypertension, myocardial ischemia, and cardiac arrhythmias. 

Somatostatin is a regulatory cyclic peptide, which has originally been described as a hypothalamic growth hormone release-inhibiting factor. It is produced throughout the central nervous system (CNS) as well as in secretoty cells of the periphery and mediates its regulatory functions on cellular processes such as neurotransmission, smooth muscle contraction, secretion and cell proliferation via a family of seven transmembrane domain G-protein-coupled receptors termed sstx 5. 

Ritodrine has an effect on beta (p)2-adrenergic receptors, principally those that innervate the uterus. Stimulation of these p2-adrenergic receptors inhibits uterine smooth muscle contractions. The pradrenergic receptors are located in the heart and are not stimulated by ritodrine when administered as prescribed. Ritodrine is used to... 

When a nerve-muscle preparation is stimulated in the presence of a sea snake neurotoxin, there is no twitch. However, when the muscle itself is stimulated directly in the presence of a neurotoxin, the muscle contracts. This means that neurotoxin does not inhibit the muscle itself. Moreover, postsynaptic neurotoxin does not inhibit the release of acetylcholine from the nerve ending. Therefore, the site of snake toxin inhibition must be in the postsynaptic site 20). Later it was shown that a neurotoxin strongly binds to the acetylcholine receptor (AChR). 

As discussed in the previous section, all the effects of the ANS in tissues and organs throughout the body, including smooth muscle contraction or relaxation alteration of myocardial activity and increased or decreased glandular secretion, are carried out by only three substances acetylcholine, norepinephrine, and epinephrine. Furthermore, each of these substances may stimulate activity in some tissues and inhibit activity in others. How can this... 

Isotonic muscle contraction was used to measure the effects of selected nematode FaRPs on the body-wall muscle of H. contortus. AF2 was found to have inhibitory effects on muscle activity and inhibited acetylcholine (ACh) -induced contractions in the worm whereas AF8 had excitatory effects on the muscle and enhanced ACh-induced contractions (Marks et al., 1999a). There were obvious differences in the methodologies used to evaluate the effects of these peptides on Haemonchus muscle compared with those used to examine these peptide effects on Ascaris. How comparable the results are has yet to be determined. 

Relaxins Inhibit smooth muscle contraction soften connective tissue (383,384)... 

Troponin C Regulates muscle contraction complex formation triggers actin to realign and interact with myosin (389,390) — inhibited by relaxins, which are themselves Ca2+-binding proteins (v.s.)... 

---