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Muscle resting potential

Equilibrium potentials calculated at 37°C from the Nernst equation. Calculated assuming a —90 mV resting potential for the muscle membrane and assuming that chloride ions are at equilibrium at rest. [Pg.97]

FIG. 5. Ca2+ sparks drive electrical activity in myocytes. In contrast to the traditional concept of electrical activity deriving from descending neural control via postsynaptic responses, spontaneous Ca2+ release results in electrical activity in smooth muscle. The figure shows a Ca2+ spark activating sarcolemmal Ca2+-activated Cl- channels and spontaneous transient inward currents (STICs) (current trace above). Whether Ca2+ sparks activate outward STOCs (Ca2+-activated K+ currents) or STICs will depend on the proportion of channels expressed and the resting potential of the myocyte. [Pg.117]

Minoxidil is a very efficacious orally active vasodilator. The effect results from the opening of potassium channels in smooth muscle membranes by minoxidil sulfate, the active metabolite. Increased potassium permeability stabilizes the membrane at its resting potential and makes contraction less likely. Like hydralazine, minoxidil dilates arterioles but not veins. Because of its greater potential antihypertensive effect, minoxidil should replace hydralazine when maximal doses of the latter are not effective or in patients with renal failure and severe hypertension, who do not respond well to hydralazine. [Pg.235]

This statement requires explanation in terms of the electrical double layer at the surface of all cells, including at the sarcolemma of myofibers and the plasma membrane of neurons. The inner part of this double layer (Stmt layer) can be regarded as a condenser with its complement of ions largely giving it a certain numerical value for permittivity (dielectric constant). This is charged when the membranes of muscle and nerve are at rest (resting potential). [Pg.326]

The long-lasting cardiac action potential is a consequence of such an evolutionary compromise in the development of potassium currents in the heart. Early work on these channels [5] showed that they could be divided into two classes channels that close on depolarization, Iki, and channels that open during depolarization, including the various components of Ik and the transient outward current, it0. At rest, Iki is switched on and holds the resting potential at a very negative level, where the other K+ currents are switched off. On depolarization iki rapidly switches off, while the other currents take time to activate and cause repolarization. This analysis of the potassium channels in cardiac muscle formed the basis of the first biophysically detailed model [6] and remains the basis of all subsequent models [7-9]. [Pg.261]

It is interesting to note that, even in the absence of lidocaine, the number of responsive channels starts to drop between the resting potential (-70 mV) and the firing level (-55 mV). From this, we would expect a slow, partial depolarization to render the membrane refiactory to excitation. This property of the Nay channels may be important in a phenomenon called depolarizing block in skeletal muscle cells. We will look into this in a later section. [Pg.50]

An intrinsic ionic charge gradient across the membrane exists because of semipermeable nature of membrane, which maintains a difference in the concentration of the ions between the cytosol and the extracellular matrix. This difference results in a definite potential across membrane of the normal cells, which is called the resting potential. Normal plant cells, mammalian muscle cells, and neurons have resting potential values of about —120, —90, and —70 mV, respectively. Along with the resistance to the flow of ions, membrane also exhibits a capacitance. Cm, which is given by... [Pg.746]

In contrast, conduction velocity is slow in muscle fibers at the SA and AV nodes. Unlike the majority of cardiac muscle cells, these pacemaker cells have an unstable resting potential ( — 60 mV) due to a cell membrane alteration that allows sodium ions to leak into the cell without a concurrent potassium ion efflux. This sodium leakage reduces the membrane potential allowing even more sodium ions to move into the cell. In addition to the inward sodium movement, there is also an inward calcium flow which causes the pacemaker cells to have a more positive resting potential. Finally, the cell produces an action potential at 40 mV. This phenomenon is called spontane-... [Pg.476]

CIC CP channels are part of a large family of anion channels, which are widely distributed throughout both eukaryotes and prokaryotes. In vertebrate skeletal muscle, CIC CP channels stabilise the resting potential and regulate electrical excitability, while in kidney, they operate to produce transepithelial fluid and electrolyte... [Pg.354]

As for the meaning of the action of avermectins in K+-free saline, Fritz et al (28) observed that when avermectin was applied in the standard lobster Ringer solution, the muscle membrane hyper-polarized by up to 5 mV within a few minutes The addition of avermectin to muscles in K+-free solution, where the resting potential is more negative than the Cl equilibrium potential, caused a depolarization of the membrane by several millivolts The suppression of influx of the avermectin-treated muscles in the K+-free... [Pg.73]


See other pages where Muscle resting potential is mentioned: [Pg.7]    [Pg.291]    [Pg.496]    [Pg.7]    [Pg.291]    [Pg.496]    [Pg.420]    [Pg.187]    [Pg.194]    [Pg.97]    [Pg.191]    [Pg.716]    [Pg.721]    [Pg.722]    [Pg.725]    [Pg.251]    [Pg.287]    [Pg.426]    [Pg.177]    [Pg.232]    [Pg.266]    [Pg.332]    [Pg.401]    [Pg.129]    [Pg.326]    [Pg.6]    [Pg.420]    [Pg.41]    [Pg.475]    [Pg.475]    [Pg.258]    [Pg.334]    [Pg.80]    [Pg.160]    [Pg.36]    [Pg.36]    [Pg.48]    [Pg.163]    [Pg.104]    [Pg.107]    [Pg.287]    [Pg.294]    [Pg.295]   
See also in sourсe #XX -- [ Pg.19 , Pg.25 ]




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