Potassium ions efflux

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-... 

Daptomycin was originally isolated from the soil saprotroph Streptomyces roseos-porus by scientists at Eli Lilly and Company in the 1980s. It is a novel lipopeptide antibiotic used in the treatment of certain infections caused by Gram-positive organisms. The proposed mechanism of action involves insertion of the lipophilic daptomycin tail into the bacterial cell membrane, causing rapid membrane depolarization and a potassium ion efflux. This leads to the arrest of DNA, RNA, and protein synthesis, resulting in bacterial cell death (see footnote 1). 

This simple technique is not applicable to ion channels that are too small or too selective to mediate the efflux of GMP. To detect the activity of ion channels with CD, the potassium selectivity of G-quartets can be used. For example, vesicles are loaded with GMP in the presence of potassium ions at concentrations above the dissociation constant ( Td) of G-quartets. In the presence of cation transporters, external cation exchange from potassium to cesium results in CD silencing as a resnlt of G-quartet disassembly within the vesicle in response to potassium ion efflux. Reversal of the direction of cation antiport with Cs-loaded vesicles and external potassium is even more attractive because the response to ion channel activity is chirogenic. This is one of the few methods where transport across and intactness of spherical membranes are simultaneously reported without additional effort (Section 4.1). 

Parasympathetic stimulation causes a decrease in heart rate. Acetylcholine, which stimulates muscarinic receptors, increases the permeability to potassium. Enhanced K+ ion efflux has a twofold effect. First, the cells become hyperpolarized and therefore the membrane potential is farther away from threshold. Second, the rate of pacemaker depolarization is decreased because the outward movement of K+ ions opposes the effect of the inward movement of Na+ and Ca++ ions. The result of these two effects of potassium efflux is that it takes longer for the SA node to reach threshold and generate an action potential. If the heart beat is generated more slowly, then fewer beats per minute are elicited. 

Sulfonylureas bind to a 140-kDa high-affinity sulfonylurea receptor (Figure 41-2) that is associated with a beta-cell inward rectifier ATP-sensitive potassium channel. Binding of a sulfonylurea inhibits the efflux of potassium ions through the channel and results in depolarization. Depolarization opens a voltage-gated calcium channel and results in calcium influx and the release of preformed insulin. 

Other optional experiments may be completed if time allows. For example, the effectiveness of various redox dyes may be analyzed. In addition to those listed in the text, FMN, ferricyanide, and dichlorophenolindophe-nol may be tested (Neumann and Jagendorf, 1964). It has been shown that NH4C1 and amines stimulate proton uptake. If a potassium ion-specific electrode is available, the light-induced efflux of K+ from spinach chloroplasts may be studied (Dilley, 1972). 

Potassium channels play an important role in the control of insulin secretion in (3-pancreatic cells. In a resting (3-pancreatic cell, the membrane potential is maintained below the threshold for insulin secretion by an efflux of potassium ions through the open potassium channels. As glucose levels rise within the cell, ATP production increases, and the change in the APT/ADP ratio leads to the closing of potassium channels. This causes the calcium channels to open, and entering calcium ions signal insulin secretion. Factors that modulate the (3-pancreatic potassium channels can fine-tune the insulin secretion. 

In type II renal tubular acidosis there is a defect in the secretion of hydrogen ions by the proximal tubule. Because the proximal tubule is the major site of bicarbonate reabsorption (4000 mEq of bicarbonate per day as compared to 70 mEq in the distal tubule), the defect in secretion of hydrogen ions in this condition leads to the flooding of the distal tubule with bicarbonate. The capacity of hydrogen ions secreted by the distal tubule to buffer this massive efflux of bicarbonate is soon overwhelmed and, as a result, large quantities of bicarbonate are excreted in the urine. Much more bicarbonate needs to be administered in this condition to correct the acidosis than is necessary in type I renal tubular acidosis. In general, in renal tubular acidosis the impairment in hydrogen ion secretion leads to excretion of potassium ions in urine. 

Akerman, K. E., Saris, N. E. Biochim. Biophys. Acta. 426 (4), 624 (1976). Stacking of safranine in liposomes during valinomycin-induced efflux of potassium ions... 

Electrical activity in the heart can be picked up by electrodes placed on the skin and recorded as the familiar electrocardiogram (ECG). The ECG is a record of the sum of all action potentials in the heart as it contracts. Action potentials are generated by depolarization followed by repolarization of the cardiac muscle cell membrane. Depolarization is initiated by an influx of sodium ions into the cardiac muscle cells, followed by an influx of calcium ions. Repolarization is brought about by efflux of potassium ions. The phases of a cardiac action potential are shown in Eigure 4.3 where the depolarization is the change in resting membrane potential of cardiac muscle cells from —90 mV to 4-20 mV. This is due to influx of sodium ions followed by influx of calcium ions. Contraction of the myocardium follows depolarization. The refractory period is the time interval when a second contraction cannot occur and repolarization is the recovery of the resting potential due to efflux of potassium ions. After this the cycle repeats itself. 

These are a relatively recent development and act by increasing the efflux of potassium ions in smooth muscle cells of blood vessels. This leads to hyperpolarization of vascular smooth muscle thereby reducing the excitability and bringing about vasodilation. The resulting vasodilation in coronary arterioles improves blood flow to the myocardium. This, in combination with a reduction in both afterload (dilation of arteries) and preload (dilation of veins), relieves the angina. Nicorandil is an example of a potassium channel activator. 

Calcium-activated potassium channels increase their permeability to potassium ions in response to increases in the intracellular calcium concentration. These potassium channels couple the membrane potential to the intracellular concentration of calcium, in that a rise in the intracellular calcium level leads to an efflux of potassium ions and hence hyperpolarization of the membrane. 

The last mediator of gastric secretion in the parietal cell is an H+,K+-ATPase (proton or acid pump) which is a member of the phosphorylating class of ion transport ATPases. Hydrolysis of ATP results in ion transport. This chemical reaction induces a conformational change in the protein that allows an electroneutral exchange of cytoplasmic H+ for K+. The pump is activated when associated with a potassium chloride pathway in the canalicular membrane which allows potassium chloride efflux into the extracytoplasmic space, and thus results in secretion of hydrochloric acid at the expense of ATP breakdown. The activity of the pump is determined by the access of K+ on this surface on the pump. In the absence of K+, the cycle stops at the level of the phosphoenzyme [137]. 

Under these conditions, a typical measured proton flux might be in the range of 10 15 mol/(cm2 s). To compare this value with that of potassium, 1 M potassium ion (as potassium sulfate) could be trapped inside the same liposomes, and potassium efflux into 1 M choline sulfate could be measured with a potassium-sensitive electrode. A typical result might again be in the range of 10 15 mol/(cm2 s). The proton permeability anomaly now becomes clear The same flux is measured for both potassium ion and protons, yet the proton flux is driven by a concentration of protons 6 orders of magnitude less than the concentration of potassium ions. Estimates of the relative permeabilities of the bilayer to protons and potassium using these flux data yield values of 10 6 cm/s for protons and 10 12 cm/s for potassium ion. 

Figure 36. Diagram illustrating movements of ions through a nerve cell membrane. The downhill movements which occur during the impulse are shown on the right uphill movements during recovery are shown on the left. The broken line represents the component of the sodium efflux which is not abolished by removing external potassium ions. (From Reference 196).

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