Na* -> K* exchange

According to the exact position of the equilibrium galvani potential for Ca2+-ions on the voltage axis, stimulation or inhibition of the Na+—K+ exchange can be understood. The effect of anions (e.g., MgATP2-) may be similiar as shown in Fig. 4. 

Figure 41-14. The transcellular movement of glucose in an intestinal cell. Glucose follows Na+ across the luminal epithelial membrane. The Na+ gradient that drives this symport is established by Na+ -K+ exchange, which occurs at the basal membrane facing the extra-ceiiuiarfiuid compartment. Glucose at high concentration within the ceii moves "downhill" into the extracel-iuiarfiuid by fadiitated diffusion (a uniport mechanism).

Figure 2. Plot of XRD peak positions (CuK radiation ethylene glycol-solvated samples) for Kinney smectite treated with 0.05 N Na + K exchange solutions. Experimental points are labeled with percentages of K in solution. The graph, used to determine percentage illite layers and glycol-spacing for illite/smectites having crystallite thickness of 1-14 layers, is from (42).

In an ion exchange kinetics study, any one or more of five steps can be rate-controlling. As an illustration of this, consider Na-K exchange on vermiculite (Sparks, 1986) ... 

The principal and intercalated cells of the collecting tubule aie responsible for Na+- K+ exchange and for H+ secretion and K+ reabsorption, respectively. Stimulation of aldosterone receptors in the principal cells results in Na+ reabsorption and K+ secretion. Antidiuretic hormone (ADH, vasopressin) receptors promote the reabsorption of water from the collecting tubules and ducts (Figure 23.3). This action is mediated by cAMP. 

Mechanism of action Spironolactone [spye row no LAK tone] is a synthetic aldosterone antagonist that competes with aldosterone for intracellular cytoplasmic receptor sites. The spironolactone-receptor complex is inactive, that is, it prevents translocation of the receptor complex into the nucleus of the target cell, and thus does not bind to DNA. This results in a failure to produce proteins that are normally synthesized in response to aldosterone. These mediator proteins normally stimulate the Na+-K+ exchange sites of the collecting tubule. Thus, a lack of mediator proteins prevents Na+ reabsorption and therefore K+ and H+ secretion. 

We wish to report a study of the cracking of n-hexane, 2-methyl-pentane, 3-methylpentane, and 2,3-dimethylbutane over K-exchanged Y, NaY, and Na,K-exchanged L zeolites at 500° and 1 atm at low conversion levels (LHSV — 0.3), as well as thermal cracking in a quartz wool-packed... 

The product mixtures over NaY and Na,K-exchanged L zeolites were indistinguishable within experimental error from those over K-exchanged Y, whereas the activities were only one-half that of K-exchanged Y. 

Acute hyperkalemia causes a hypopolarization of the cardiac muscle cell membrane, resulting in characteristic electrocardiographic changes followed by serious and often fatal arrhythmias in most cases there are no warning symptoms. Immediate treatment is needed and consists of giving sodium bicarbonate, glucose, and insulin intravenously to shift K+ into the cells calcium intravenously to minimize the cardiotoxicity of hyperkalemia and polysterene sodium (a Na/K exchange resin) rectally or orally to remove potassium from the body if all fails, the performance of dialysis may be required (S18). 

For the purposes of this article, the most important ion transport systems are those involving Na+, K+, and Ca +. Transport systems for neurotransmitters will be discussed subsequently. Most probably Cl is distributed across the axolemma passively, and because the concentration of Mg + appears to be very similar in both extra- and intracellular compartments, the active transport of this cation has not received close scrutiny. Hence, the Na" "—K+ exchange system and systems involved in the transport of Ca " " will receive primary attention. Excellent reviews on the transport of Na+ and K" " will be found in Skou and Norby (1979) an excellent source on calcium transport and its intracellular roles can be found in Scarpa and Carafoli (1978). 

Effects on the Na pump of erythrocytes when the membrane cholesterol is depleted have been demonstrated. influx was reduced [84] whereas other workers have reported increased Na efflux [85] and increased selectivity of the pump for internal Na [86]. We have simultaneously measured Na" and transport via the Na -K pump in thymocytes [87,88]. Cholesterol depletion activated pump-mediated Na efflux but inhibited pump-mediated influx, whereas under normal physiological conditions these two fluxes are stoichiometrically linked [88-90]. Furthermore, the mode of functioning of the pump was altered, i.e. Na -Na exchange instead of the normal Na -K" exchange occurred. It was suggested that in this case cholesterol depletion may cause molecular rearrangements of the multimeric enzyme protein within the phospholipid bilayer [89]. 

Figure 5.12 Transport proteins in cell membranes, (a) Energy-dependent, ATP-powered ion pumps such as the Na /K exchange ATPase (b) channels, gated or non-gated, which permit diffusion through an aqueous pathway, such as voltage-gated Na channels (c) passive, facilitated transport systems, which can act in uniport, symport, or antiport modes, such as the glucose transporter. The filled arrow indicates gradient of molecules indicated by the filled symbol.

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