Activation hyperpolarized dependence

Recent work using confocal microscopy has found localized increases of [Ca2+]j named Ca2+ sparks which are due to the release of Ca2+ from one or a small number of RyRs (Jaggar et al 2000). These localized releases of Ca2+ activate Ca2+-dependent channels in the surface membrane (Perez et al 2001). Activation of the Ca2+-activated K+ current will hyperpolarize the membrane potential (Herrera et al 2001) and thereby decrease Ca2+ entry into the cell on voltage-dependent Ca2+ channels. This provides a mechanism whereby Ca2+ release from the SR can decrease contraction. It is therefore important, in different smooth muscles, to consider to what extent SR Ca2+ release activates rather than decreases contraction. It is, of course, possible that, in the same smooth muscle, SR release may sometimes directly activate contraction and, at other times, decrease it by activating K+ channels. 

Mode of action of opioids. Most neurons react to opioids with hyperpolarization, reflecting an increase in 1C conductance. Ca influx into nerve terminals during excitation is decreased, leading to a decreased release of excitatory transmitters and decreased synaptic activity (A), Depending on the cell population affected, this synaptic inhibition translates into a depressant or excitant effect (B),... 

Finally, what matters most from the physiological point of view is that direct calcium entry through nicotinic receptors can be sufficient to act as a postsynaptic signal, for instance, activating calcium-dependent SK potassium channels in outer hair cells of the cochlea (154) or contributing to apamin-sensi-tive hyperpolarization in rat otic ganglion (155). 

Fig. 19.2 Summary of polyamine effects on ion transport across the plasma and vacuolar mem-brtmes in plants. I. PAs directly and with a high affinity inhibited nonselectiveFV channels, whereas K -selective VK channels are almost unaffected. 2. PAs caused an indirect low-affinity inhibition of the PM K (inward and outward rectifying, KIRC and KORC) and weakly voltage dependent non-selective cation (Vl-NSCC) channels. 3. ROS-mediated effects of PAs on the PM ion channels ROS production is initiated by PAs export to the apoplast and oxidation by polytunine oxidases (PAOs) and/or diamine (DAOs) oxidases, yielding H2O2. ROS activate hyperpolarization-activated Ca ...

In the following, the cardiac action potential is explained (Fig. 1) An action potential is initiated by depolarization of the plasma membrane due to the pacemaker current (If) (carried by K+ and Na+, which can be modulated by acetylcholine and by adenosine) modulated by effects of sympathetic innervation and (3-adrenergic activation of Ca2+-influx as well as by acetylcholine- or adenosine-dependent K+-channels [in sinus nodal and atrioventricular nodal cells] or to dqjolarization of the neighbouring cell. Depolarization opens the fast Na+ channel resulting in a fast depolarization (phase 0 ofthe action potential). These channels then inactivate and can only be activated if the membrane is hyperpolarized... 

A shift of the voltage-dependence of inactivation to a hyperpolarizing direction, resulting in a lower fraction of channels available for activation at action potential threshold. 

Membrane depolarization typically results from an increase in Na+ conductance. In addition, mobilization of intracellular Ca2+ from the endoplasmic or sarcoplasmic reticulum and the influx of extracellular Ca2+ appear to be elicited by ACh acting on muscarinic receptors (see Ch. 22). The resulting increase in intracellular free Ca2+ is involved in activation of contractile, metabolic and secretory events. Stimulation of muscarinic receptors has been linked to changes in cyclic nucleotide concentrations. Reductions in cAMP concentrations and increases in cGMP concentrations are typical responses (see Ch. 21). These cyclic nucleotides may facilitate contraction or relaxation, depending on the particular tissue. Inhibitory responses also are associated with membrane hyperpolarization, and this is a consequence of an increased K+ conductance. Increases in K+ conductance may be mediated by a direct receptor linkage to a K+ channel or by increases in intracellular Ca2+, which in turn activate K+ channels. Mechanisms by which muscarinic receptors couple to multiple cellular responses are considered later. 

A parameter (usually symbolized by P, and often containing a subscript to indicate the specific ion) that is a measure of the ease with which an ion can cross a unit area of membrane by simple (or passive) diffusion through a membrane experiencing a 1.0 M concentration gradient. For a particular biological membrane, the permeabilities are dependent on the concentration and activity of various channel or transporter proteins. In an electrically active cell (e.g., a neuron), increasing the permeability of K+ or CF will usually result in hyperpolarization of the membrane. Increasing will cause depolarization. 

Minoxidil (Loniten) is an orally effective vasodilator. It is more potent and longer acting than hydralazine and does not accumulate significantly in patients with renal insufficiency. It depends on in vivo metabolism by hepatic enzymes to produce an active metabolite, minoxidil sulfate. Minoxidil sulfate activates potassium channels, resulting in hyperpolarization of vascular smooth muscle and relaxation of the blood vessel. 

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