Muscle contraction study

In the PNS, the neuromuscular junction (NMJ) is an interface between neurons and the muscle end plate responsible for initiating muscle contraction. Studies have found that NMJs are embedded in basal lamina, which is composed of laminin, heparin sulfate proteoglycans (HSPGs), CSPGs (ie, versican, brevican, neurocan), and collagen IV, the most abundant ECM molecule at the NMJ synapse (Barros et al., 2011 Patton, 2003). 

Guia Rosaa, M. A. Cavalcanti Garcia, M. N. Souzaa, A novel electromyographic signal simulator for muscle contraction studies, Computer methods and pn rams in biomedicine 89, 269-274, 2008... 

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... 

Fisher, A., Smith, C., Thoden, J., et al., 1995. Structural studies of myosin nncleotide complexes A revised model for die molecular basis of muscle contraction. Biophysical Journal... 

Studies on muscle contraction carried out between 1930 and 1960 heralded the modem era of research on cytoskeletal stmctures. Actin and myosin were identified as the major contractile proteins of muscle, and detailed electron microscopic studies on sarcomeres by H.E. Huxley and associates in the 1950s produced the concept of the sliding filament model, which remains the keystone to an understanding of the molecular mechanisms responsible for cytoskeletal motility. 

Asthma is a complex respiratory disorder that involves mast cell degranulation, mucous secretions, and smooth muscle hypertrophy and hyperresponsiveness. Smooth muscle hyperresponsiveness has suggested some defect in the regulation of smooth muscle contractility. Therefore, a number of studies concerning asthma have centered on whether alterations in the regulation of smooth muscle contraction (Figure 4) are responsible for hyperactivity in asthmatic airway smooth muscle. 

Vascular Effects of Complement Activation. During complement activation a number of complement fragments (anaphylatoxins), which are polypeptides with inflammatory properties, are released. The anaphylatoxins C3a and C5a induce smooth muscle contraction and enhance vascular permeability (H31). The most pronounced activation of complement with the formation of anaphylatoxins and terminal C5-9 complexes has been observed in septic shock (B29, B30, P2). Studies indicate that there is a relation between high concentrations of anaphylatoxins and C5-9 complexes and the development of ARDS or MODS in patients with sepsis (H10). 

An initial hint that Ca2+ stores are present and functional in smooth muscle cells came from earlier experiments revealing that agonist-induced contractions could be observed in the absence of extracellular Ca2+. It is now known that smooth muscle Ca2+ stores express two types of Ca2+ release channels, the ryanodine receptor (RyR) and the inositol-1,4,5-trisphosphate (L1SP3) receptor (L1SP3R) (Somlyo Somlyo 1994). Recent studies have shown that Ca2+ release from intracellular Ca2+ stores plays various important roles in the regulation of smooth muscle contraction. Local and transient releases of Ca2+ from RyR near the surface membrane, which are called Ca2+ sparks, activate Ca2+-sensitive K+... 

Raeymaekers L, Wuytack F 1996 Calcium Pumps. In Barany M (ed) Biochemistry of smooth muscle contraction. Academic Press, New York, p 241-253 Shull GE 2000 Gene knockout studies of Ca2+-transporting ATPases. Eur J Biochem 267 5284-5290... 

Claude Bernard s early discovery (1856) that curare, the South American arrow poison (woorari), blocked muscle contraction elicited by stimulation of motor neurons, but not that elicited by direct stimulation of the muscle, provided the first demonstration that drugs could be used to study, what we now know are, nAChR-regulated functions. Bernard s early experiment served as the model for Langley s demonstration that the actions of nicotine on skeletal muscle could be blocked by pretreatment with curare (Langley 1880, 1907) and mimicked by pituri, the active... 

This muscle phosphotransferase (EC 2.132) catalyzes the reversible rephosphorylation of ADP to form ATP (/.c., T eq = [ATP][Creatine]/([Creatine phosphate] [ADP]) = 30). In resting muscle, creatine phosphate is synthesized at the expense of abundant stores of ATP intracellular creatine phosphate stores often reach 50-60 mM. If ATP is suddenly depleted by muscle contraction, its product ADP is immediately converted back into ATP by the reverse of the creatine kinase reaction. Depending on the pH at which the enzyme is studied, the kinetic reaction can be either rapid equilibrium random or rapid equilibrium ordered. A-Ethylglycocyamine can also act as a substrate. 

Muscles contract and expand in response to electrical, thermal, and chemical stimuli. Certain polymers, such as synthetic polypeptides, are known to change shape on application of electric current, temperature, and chemical environment. For instance, selected bioelastic smart materials expand in salt solutions and may be used in desalination efforts and as salt concentration sensors. Polypeptides and other polymeric materials are being studied in tissue reconstruction, as adhesive barriers to prevent adhesion growth between surgically operated tissues, and in controlled drug release, where the material is designed to behave in a predetermined matter according to a specific chemical environment. 

Diazoxide is an effective and relatively long-acting parenterally administered arteriolar dilator that is occasionally used to treat hypertensive emergencies. Injection of diazoxide results in a rapid fall in systemic vascular resistance and mean arterial blood pressure associated with substantial tachycardia and increase in cardiac output. Studies of its mechanism suggest that it prevents vascular smooth muscle contraction by opening potassium channels and stabilizing the membrane potential at the resting level. 

---