Extracellular potassium ions

Sick T. J., Tang R., and Perez-Pinzon M. A. (1999) Cerebral blood flow does not mediate the effect of brain temperature on recovery of extracellular potassium ion activity after transient focal ischemia in the rat. Brain Res. 821,400-406. 

While there has been considerable interest in the ionic changes that occur during focal ischemia, little attention has been paid to disturbances associate with reperfusion. Most earlier investigations, for example, have shown that extracellular potassium ion activity recovers to or near preischemic levels on reperfusion (29,37), suggesting normalization of potassium ion homeostasis. We have recently shown, however, that focal ischemia is accompanied by early secondary elevation of extracellular potassium ion activity that is dependent on brain temperature but not cerebral blood flow (38). 

Lantos J., Temes G., andTorokB. (1986) Changes during ischaemia in extracellular potassium ion concentration of the brain under nitrous oxide or hexobarbital-sodium anaesthesia and moderate hypothermia. Acta Physiol. Hung. 67,141-153. 

The mechanism of Step 2 indicates that extracellular potassium ions are required for acid secretion. Food is a reliable source oi potassium ions however, a basal level of acid secretion may occur in the absence of food and the cephalic phase can result in add secretion in the absence of food. Therefore, the cell must supply its own potassium ions, as shown in Step 3. 

The major regulators of aldosterone secretion are the renin-angiotensin system and extracellular potassium ions (K+). The former is sensitive to changes in intravascular volume and arterial pressure, while the latter is an aldosterone-regulated substance that feeds back to reduce aldosterone synthesis (simple negative feedback). Aldosterone secretion is also influenced (but not regulated) by ACTH and, directly and indirectly, by atrial natriuretic factor (ANF). 

Conversely, metabolic alkalosis results in hypokalemia as a result of a net loss of hydrogen ion in the serum. In response, the body releases intracellular hydrogen ion into the serum to increase the acidity of the blood in exchange for extracellular potassium ions. This creates a relative deficiency of serum potassium. Serum potassium falls approximately 0.6 mEq/L for each 0.1 unit rise in blood pH. Similarly, this is frequently termed false hypokalemia because there isn t a true deficiency in total body potassium. 

The Na,K ATPase exchanges intracellular sodium ions for extracellular potassium ions, the gastric ATPase H3O for extracellular potassium, and the sarcoplasmic or endoplasmic reticular Ca pump two cytoplasmic Ca for 2H in the sarcoplasmic reticulum. In the outward reaction transporting Na% H% or Ca % the catalytic subunit is phosphorylated by ATP, and in the inward reaction, the phosphoenzyme is dephosphorylated by K or H (in the case of the sarcoplasmic reticulum Ca ATPase). To achieve uphill transport at a significant rate, there has to be a decrease in binding-site affinity on the side of the membrane from which the ion is transported and reorientation of this site toward the side to which the ion is transported. 

Sodium and Potassium. Whereas sodium ion is the most abundant cation in the extracellular fluid, potassium ion is the most abundant in the intracellular fluid. Small amounts of K" are requited in the extracellular fluid to maintain normal muscle activity. Some sodium ion is also present in intracellular fluid (see Fig. 5). Common food sources rich in potassium may be found in Table 7. Those rich in sodium are Hsted in Table 8. 

The ventricular action potential is depicted in Fig. 6-2.2 Myocyte resting membrane potential is usually -70 to -90 mV, due to the action of the sodium-potassium adenosine triphosphatase (ATPase) pump, which maintains relatively high extracellular sodium concentrations and relatively low extracellular potassium concentrations. During each action potential cycle, the potential of the membrane increases to a threshold potential, usually -60 to -80 mV. When the membrane potential reaches this threshold, the fast sodium channels open, allowing sodium ions to rapidly enter the cell. This rapid influx of positive ions... 

An intracellular to extracellular difference in sodium and potassium ion concentrations is essential to the function of nerves, transport of important nutrients into the cell, and maintenance of proper cell volume. 

Solis JM, Herranz AS, Herreras O, Munoz MD, Martin del Rio R, et al. 1986. Variation of potassium ion concentrations in the rat hippocampus specifically affects extracellular taurine levels. Neurosci Lett 66(3) 263-268. 

The basic answer to this question is that ions move across the plasma membrane of the neuron. Recall that ions are charged particles, frequently derived from single atoms by the gain or loss of electrons. The ions that are most important to us in understanding nervous system function are sodium ion, Na+, potassium ion, K+, calcium ion, Ca +, and chloride ion, Cl . If we compare the concentrations of these ions on the inside of the neuron and in the extracellular fluid that bathes the neuron, we find the neuron interior has a higher concentration of potassium ion than does the exterior fluid. In contrast, the exterior fluid has higher concentrations of sodium, calcium, and chloride ions than does the neuron interior. These concentration differences are referred to as concentration gradients. 

In pacemaker cells (whether normal or ectopic), spontaneous depolarization (the pacemaker potential) occurs during diastole (phase 4, Figure 14-1). This depolarization results from a gradual increase of depolarizing current through special hyperpolarization-activated ion channels (If, also called If,) in pacemaker cells. The effect of changing extracellular potassium is more complex in a pacemaker cell than it is in a nonpacemaker cell because the effect on permeability to potassium is much more important in a pacemaker (see Effects of Potassium). In a pacemaker—especially an ectopic one—the end result of an increase in extracellular potassium is usually to slow or stop the pacemaker. Conversely, hypokalemia often facilitates ectopic pacemakers. 

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