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Membrane potential calcium channels

The resting membrane potential of most excitable cells is around —60 to —80 mV. This gradient is maintained by the activity of various ion channels. When the potassium channels of the cell open, potassium efflux occurs and hyperpolari2ation results. This decreases calcium channel openings, which ia turn preveats the influx of calcium iato the cell lea ding to a decrease ia iatraceUular calcium ia the smooth muscles of the vasculature. The vascular smooth muscles thea relax and the systemic blood pressure faUs. [Pg.143]

Lee, K.S., Marban, E. and Tsien, R.W. (1985). Inactivation of calcium channels in mammalian heart cells joint dependence on membrane potential and intracellular calcium. J. Physiol. 364, 395-411. [Pg.71]

When the action potential reaches the synaptic bouton, depolarisation triggers the opening of voltage-operated calcium channels in the membrane (Figure 2.5). The concentration gradient for Ca2+ favours the passive movement of this ion into the neuron. The subsequent rise in cytoplasmic Ca2+ ion concentration stimulates the release of neurotransmitter into the synaptic cleft, which diffuses across this narrow gap and binds to receptors located on the postsynaptic neuronal membrane (Figure 2.5). [Pg.17]

Several different changes in mitochondria occur during apoptosis. These include a change in membrane potential (usually depolarization), increased production of reactive oxygen species, potassium channel activation, calcium ion uptake, increased membrane permeability and release of cytochrome c and apoptosis inducing factor (AIF) [25]. Increased permeability of the mitochondrial membranes is a pivotal event in apoptosis and appears to result from the formation of pores in the membrane the proteins that form such permeability transition pores (PTP) may include a voltage-dependent anion channel (VDAC), the adenine nucleotide translocator, cyclophilin D, the peripheral benzodiazepine receptor, hexokinase and... [Pg.610]

Fig. 4.1. Cellular model illustrating cell types in vascular wall involved in vasorelaxation induced by SERMs. Putative targets of SERMs are indicated within cyan tags. SERMs directly affect L-type VDCC, BK fil subunit in smooth muscle cells, and ER in endothelial cells. L-type VDCC L-type voltage-dependent calcium channel BK calcium-activated large conductance K+ channel PKG protein kinase G eNOS endothelial nitric oxide synthase GC soluble guanylate cyclase cGMP cyclic GM P V electrochemical membrane potential ER estrogen receptor. See text for further details... Fig. 4.1. Cellular model illustrating cell types in vascular wall involved in vasorelaxation induced by SERMs. Putative targets of SERMs are indicated within cyan tags. SERMs directly affect L-type VDCC, BK fil subunit in smooth muscle cells, and ER in endothelial cells. L-type VDCC L-type voltage-dependent calcium channel BK calcium-activated large conductance K+ channel PKG protein kinase G eNOS endothelial nitric oxide synthase GC soluble guanylate cyclase cGMP cyclic GM P V electrochemical membrane potential ER estrogen receptor. See text for further details...
Some of the main types of cellular regulation associated with rhythmic behavior are listed in Table III. Regulation of ion channels gives rise to the periodic variation of the membrane potential in nerve and cardiac cells [27, 28 for a recent review of neural rhythms see, for example, Ref. 29]. Regulation of enzyme activity is associated with metabolic oscillations, such as those that occur in glycolysis in yeast and muscle cells. Calcium oscillations originate... [Pg.257]

In sum, the natural tendency will be for sodium, calcium, and chloride ions to flow into the neuron and for potassium ions to flow out, and in so doing to reduce the membrane potential to zero. In reality, this is not so easy. The plasma membrane of the neuron is not very permeable to these ions. If it were, it would be impossible to sustain concentration gradients across it. The rate of passive diffusion of these ions across this membrane is very slow, though not zero, and different for each ion. So how do ions get across the neuronal plasma membrane rapidly There are two ways gated channels and active transport by pumps. [Pg.289]

A next-level assay is usually an isolated heart/cardiac tissue preparation. The canine Purkinje fiber assay (GLP) measures several action potential parameters, like resting membrane potential, upstroke velocity, action potential duration and shape, but also if a drug acts reverse-use dependently [72]. Based on changes of the action potential shape it is possible to conclude which ion channels are modulated (e.g., L-type calcium channel block would abolish the plateau phase). The papillary muscle assay (e.g., guinea pigs) determines similar parameters [73]. [Pg.396]


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Membrane potential

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