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Muscle-cell membrane

Smooth muscle cell activity is in general under neural control. Thus, the many transmitters of the autonomic nervous system are paired with receptors on the smooth muscle cell membrane. One of the current questions about smooth muscle function is What intracellular processes are the different transmitters modulating in the smooth muscle cells, in addition to their effects on the contractile state ... [Pg.156]

Voluntary muscle contraction is initiated in the brain-eliciting action potentials which are transmitted via motor nerves to the neuromuscular junction where acetylcholine is released causing a depolarization of the muscle cell membrane. An action potential is formed which is spread over the surface membrane and into the transverse (T) tubular system. The action potential in the T-tubular system triggers Ca " release from the sarcoplasmic reticulum (SR) into the myoplasm where Ca " binds to troponin C and activates actin. This results in crossbridge formation between actin and myosin and muscle contraction. [Pg.240]

Motor end-plate or neuromuscular junction = axon terminal in apposition to specialized surface of muscle cell membrane... [Pg.92]

Muscle cell membranes of nematodes possess ion channel receptors that are opened by neurotransmitters and which are gated by selective therapeutic agents. This chapter is an introduction to the physiology and pharmacology of ligand-gated ion channels of nematode muscle. [Pg.449]

Fig. 21.3. Two-micropipette current-clamp recording and effect of maintained application of 30 pM levamisole, which produces a 15 mV depolarization (upward movement of trace). The downward transients are the result of injected current pulses used to measure membrane conductance. The trace gets narrower as the input conductance increases from 2.35 pS to 4.35 pS as the levamisole ion channels open. The peak amplitude of the membrane potential response and change in input conductance are used as an assay of the number and activity of the levamisole ion channel receptors present in the muscle cell membrane. The response was fully reversible on washing (not shown). Fig. 21.3. Two-micropipette current-clamp recording and effect of maintained application of 30 pM levamisole, which produces a 15 mV depolarization (upward movement of trace). The downward transients are the result of injected current pulses used to measure membrane conductance. The trace gets narrower as the input conductance increases from 2.35 pS to 4.35 pS as the levamisole ion channels open. The peak amplitude of the membrane potential response and change in input conductance are used as an assay of the number and activity of the levamisole ion channel receptors present in the muscle cell membrane. The response was fully reversible on washing (not shown).
Dubey RK, Tyurina YY, Tyurin VA, Gillespie DG, Branch RA, Jackson EK, Kagan VE (1999) Estrogen and tamoxifen metabolites protect smooth muscle cell membrane phospholipids against peroxidation and inhibit cell growth. Circ Res 84 229-239... [Pg.239]

The SR may contribute to excitation-contraction (EC) coupling in two ways firstly, by the release of Ca2+ for contraction as described above, but secondly by modulating membrane excitability. As will be described elsewhere in this book, the SR is an important mediator of surface membrane ion channel activity, and hence, excitability. Spontaneous Ca2+ release from the SR can activate Ca2+-sensitive ion channels. Both K+ (Kca) and Cl- (Clsmooth muscle cell membrane can be activated by SR Ca2+. If Kca channels are activated there will be a hyperpolarization, as K+ ions leave the cell and spontaneous transient outward currents (STOCs) can be recorded (Carl et al 1996, Nelson Quayle... [Pg.212]

Succinylcholine is degraded more slowly than is ACh and therefore remains in die synaptic cleft for several minutes, causing an endplate depolarization of corresponding duration. This depolarization initially triggers a propagated action potential (AP) in the surrounding muscle cell membrane, leading to contraction of the muscle fiber. After its i.v. injection, fine muscle twitches (fascicu-lations) can be observed. A new AP can be elicited near the endplate only if the membrane has been allowed to repolarize. [Pg.186]

Uterine relaxation is mediated in part through inhibition of MLCK. This inhibition results from the phosphorylation of MLCK that follows the stimulation of myometrial (3-adrenoceptors relaxation involves the activity of a cyclic adenosine monophosphate (cAMP) mediated protein kinase, accumulation of Ca++ in the sarcoplasmic reticulum, and a decrease in cytoplasmic Ca. Other circulating substances that favor quiescence of uterine smooth muscle include progesterone, which increases throughout pregnancy, and possibly prostacyclin. Progesterone s action probably involves hyperpolarization of the muscle cell membrane, reduction of impulse conduction in muscle cells, and increased calcium binding to the sarcoplasmic reticulum. [Pg.718]

Mechanism of Action An antihypertensive that inhibits calcium movement across cardiacand vascular smooth-muscle cell membranes. Therapeutic Effect Relieves angina by dilating coronary arteries, peripheral arteries, and arterioles. Decreases total peripheral vascular resistance and BP by vasodilation. [Pg.62]

Mechanism of Action A cerebral vasospasm agent that inhibits movement of calcium ions across vascular smooth-muscle cell membranes, T herapeuticEffect Produces fa-... [Pg.869]

The chemical synapse is a highly specialized structure that has evolved for exquisitely controlled voltage-dependent secretions. The chemical messengers, stored in vesicles, are released from the presynaptic cell following the arrival of an action potential that triggers the vesicular release into the presynaptic terminal. Once released from the vesicles, the transmitter diffuses across a narrow synaptic cleft, then binds to specific receptors in the postsynaptic cell, and finally initiates an action potential event in the nerve-muscle cell membrane by triggering muscle contractions. [Pg.223]

Fig. 4. Structure of striated muscle costameres and the DPC. A single membrane-associated costamere from a portion of a striated muscle fiber is magnified above to show the components of the dystrophin-associated protein complex that are involved in linking desmin intermediate filaments (IFs) to the muscle cell membrane. Additional actin-associated proteins present at these sites (including vinculin, talin, spectrin, and ankyrin) are not shown here. In addition to components of the DPC, plectin has also been localized to costameres, and likely contributes to linking desmin IFs to actin-associated structures. Fig. 4. Structure of striated muscle costameres and the DPC. A single membrane-associated costamere from a portion of a striated muscle fiber is magnified above to show the components of the dystrophin-associated protein complex that are involved in linking desmin intermediate filaments (IFs) to the muscle cell membrane. Additional actin-associated proteins present at these sites (including vinculin, talin, spectrin, and ankyrin) are not shown here. In addition to components of the DPC, plectin has also been localized to costameres, and likely contributes to linking desmin IFs to actin-associated structures.
When Creatine is ingested 45-90 minutes before a work-out, an athlete can take advantage of the training induced increases in blood flow to muscle tissue to transport essential nutrients across muscle cell membranes. (This also acts as a buffer to lactic acid) Since high intensity work-outs trigger the release of adrenal hormones such as Epinephrine and Norepinephrine, the cellular uptake of nutrients is improved. Remember, Ephedrine increases cellular uptake Well Ephedrine is an Epinephrine Mimicker. [Pg.217]

Administration of muscarinic agonists, like parasympathetic nervous system stimulation, increases the secretory and motor activity of the gut. The salivary and gastric glands are strongly stimulated the pancreas and small intestinal glands less so. Peristaltic activity is increased throughout the gut, and most sphincters are relaxed. Stimulation of contraction in this organ system involves depolarization of the smooth muscle cell membrane and increased calcium influx. [Pg.135]

Orida, N. Poo, M.-M. Electrophoretic movement and localisation of acetylcholine receptors in the embryonic muscle cell membrane. Nature 1978, 275, 31-35. [Pg.296]

Seki N, Suzuki H (1990) Electrical properties of smooth muscle cell membrane in renal pelvis of rabbits. Am J Physiol 259 (Renal, Fluid, Electrolyte Physiol 28) F888-F894... [Pg.136]

In muscular dystrophy, therefore, the maintenance of considerable serum activities of soluble enzymes almost certainly of sarcoplasmic origin, and known to be subject to very rapid and continuous clearance from serum, strongly argues their ceaseless copious discharge from dystrophic muscle. The likelihood at once arises that the dystrophic muscle cell membrane is unduly permeable to these enzymes, that their activities are diminished within the cell, and that because of such lavish discharge even reduced intracellular activities could be preserved only by unusually rapid renewal. These probabilities receive substantial support from the results obtained by other workers. [Pg.151]

B. across muscle cell membranes during strenuous exercise... [Pg.106]


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See also in sourсe #XX -- [ Pg.289 ]




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