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PubMed1989

[Further research on the role of prostanoids in controlling renal function in humans in normal potassium balance and acute experimental potassium depletion. I: Studies of normal potassium balance. Effects of indomethacin].

The renal function was studied by clearance (cl.) method during hypotonic polyuria (oral water load followed by 5% dextrose solution infusion) and successive relative antidiuresis induced by lysine-8-vasopressin (LVP) administration (5 microU in bolo followed by continuous infusion at a rate of 0.04 microU/min). Four 15 min and two 60 min clearance (cl.) periods were performed during hypotonic polyuria and antidiuresis, respectively. Glomerular filtration rate was estimated by creatinine cl.; the osmotic cl. (Cosm, CH2O), the absolute and fractional excretions of water, sodium, potassium and chloride were determined by usual methods. The urinary PGE2, 6-keto-PGF1 alpha and TxB2 concentrations were determined by RIA method. Fourteen healthy women submitted to a normal sodium and potassium daily intake were studied; in 6 of them paired studies in absence and in presence of indomethacin (100 mg, i.m.), respectively, were performed. LVP induced a significant reduction of creatinine cl., urinary flow rate and of prostanoid excretion. In hypotonic polyuria, indomethacin significantly reduced the creatinine cl. and the diuretic response to the water load; moreover the urinary PGE2 and 6-keto-PGF1 alpha excretions were significantly lower (85.6 +/- 1.9% and 37.7 +/- 3.2%) while the reduction of urinary TxB2 excretion was not significant (34.4 +/- 13%). Indomethacin did not affect significantly the LVP renal effects in normal potassium balance.

Dinoprostone↗
PubMed1999

Dietary potassium bicarbonate and potassium citrate have a greater inhibitory effect than does potassium chloride on magnesium absorption in wethers.

We addressed the question whether the type of anion in potassium salts affects magnesium absorption and the transmural potential difference by using wethers (n = 8) fed a control diet and diets supplemented with equimolar amounts of KHCO(3), KCl or K-citrate according to a Latin-square design. The control diet contained 10.9 g K/kg dry matter and the high K diets contained 41.3 g K/kg dry matter. Compared with the control diet, KHCO(3) and K-citrate significantly reduced apparent Mg absorption by 9.5 and 6.5%, respectively. Supplemental KCl tended to reduce (P = 0.070) group mean magnesium absorption by 5.5%. Consumption of supplemental KHCO(3) and K-citrate produced a significant increase in the transmural potential difference (serosal side = positive) by 17.1 and 20.7 mV, respectively, whereas the addition of KCl to the diet did not. The individual values for the four diets tended to show a negative correlation (r = -0.336, n = 32, P = 0.060) between the transmural potential difference and apparent magnesium absorption. We conclude that different potassium salts have different effects on magnesium absorption in ruminants as caused by different effects on the transmural potential difference.

Animals↗
PubMed1971

Active sodium and potassium transport in high potassium and low potassium sheep red cells.

The kinetic characteristics of the ouabain-sensitive (Na + K) transport system (pump) of high potassium (HK) and low potassium (LK) sheep red cells have been investigated. In sodium medium, the curve relating pump rate to external K is sigmoid with half maximal stimulation (K(1/2)) occurring at 3 mM for both cell types, the maximum pump rate in HK cells being about four times that in LK cells. In sodium-free media, both HK and LK pumps are adequately described by the Michaelis-Menten equation, but the K(1/2) for HK cells is 0.6 +/- 0.1 mM K, while that for LK is 0.2 +/- 0.05 mM K. When the internal Na and K content of the cells was varied by the PCMBS method, it was found that the pump rate of HK cells showed a gradual increase from zero at very low internal Na to a maximum when internal K was reduced to nearly zero (100% Na). In LK cells, on the other hand, no pump activity was detected if Na constituted less than 70% of the total (Na + K) in the cell. Increasing Na from 70 to nearly 100% of the internal cation composition, however, resulted in an exponential increase in pump rate in these cells to about (1/6) the maximum rate observed in HK cells. While changes in internal composition altered the pump rate at saturating concentrations of external K, it had no effect on the apparent affinity of the pumps for external K. These results lead us to conclude that the individual pump sites in the HK and LK sheep red cell membranes must be different. Moreover, we believe that these data contribute significantly to defining the types of mechanism which can account for the kinetic characteristics of (Na + K) transport in sheep red cells and perhaps in other systems.

Animals↗
PubMed1974

A kinetic description for sodium and potassium effects on (Na+ plus K+)-adenosine triphosphatase: a model for a two-nonequivalent site potassium activation and an analysis of multiequivalent site models for sodium activation.

1. Dissociation constants for sodium and potassium of a site that modulates the rate of ouabain-(Na(+)+K(+))-ATPase interaction were applied to models for potassium activation of (Na(+)+K(+))-ATPase. The constants for potassium (0.213 mM) and for sodium (13.7 mM) were defined, respectively, as activation constant, K(a) and inhibitory constant, K(i).2. Tests of the one- and the two-equivalent site models, that describe sodium and potassium competition, revealed that neither model adequately predicts the activation effects of potassium in the presence of 100 or 200 mM sodium.3. The potassium-activation data, obtained at low potassium and high sodium, were explained by a two-nonequivalent site model where the dissociation constants of the first site are 0.213 mM for potassium and 13.7 mM for sodium. The second site was characterized by dissociation constants of 0.091 mM for potassium and 74.1 mM for sodium.4. The two-nonequivalent site model adequately predicted the responses to concentrations of potassium between 0.25 and 5 mM in the presence of 100-500 mM sodium. At lower sodium concentrations the predicted responses formed an upper limit for the function of observed activities. This limit was reached at lower concentrations of potassium and higher concentrations of sodium, which inferred saturation of the sodium-activation sites with sodium.5. Sodium-activation data were corrected for sodium interaction with potassium-activation sites by use of the two-nonequivalent site model for potassium activation. Tests of equivalent site models suggested that the corrected data for sodium activation may be most consistent with a model that has three-equivalent sites. Other multiequivalent site models (n = 2, 4, 5 or 6), however, cannot be statistically eliminated as possibilities. The three-equivalent site activation model was characterized by dissociation constants of 1.39 mM for sodium and 11.7 mM for potassium. The system theoretically would be half-maximally activated by 5.35 mM sodium in the absence of potassium.6. Derivation of the model for sodium activation assumed that the affinities of these sites for sodium and potassium are independent of cation interactions with the potassium-activation sites. Therefore, the kinetic descriptions for sodium and potassium effects form a composite model that is consistent with simultaneous transport of sodium and potassium.7. Predictions of the composite equation are in reasonable agreement with data obtained by variation of sodium (potassium = 10 mM), variation of potassium (sodium = 100 mM) and by simultaneous variation of sodium and potassium (sodium:potassium = 10). Sodium-activation data (2.5-20 mM sodium) also agree with predictions of the model in the presence of potassium concentrations which are thought to be present at the sodium-activation sites in vivo.8. The kinetic description for sodium (three-equivalent sites) and potassium (two-nonequivalent sites) activation of the transport-ATPase is in accord with the probable stoichiometric requirements of the sodium pump. The model is also in general agreement with other studies on intact transporting systems and (Na(+)+K(+))-ATPase in fragmented membrane preparations with respect to potassium activation, although there is a quantitative disagreement. The model for sodium activation, though consistent with data obtained by other studies on fragmented (Na(+)+K(+))-ATPase preparations, is in apparent variance with much of the data obtained for intact transporting systems. The description for potassium activation suggests that the rates of ouabain binding to (Na(+)+K(+))-ATPase are modulated by competition between sodium and potassium for one of the two potassium-activation sites.

Adenosine Triphosphatases↗
PubMed2005

Effect of short-term supplementation of potassium chloride and potassium citrate on blood pressure in hypertensives.

Randomized trials have shown that increasing potassium intake lowers blood pressure. However, most previous trials used potassium chloride, whereas potassium in fruits and vegetables is not a chloride salt. It is unclear whether a nonchloride salt of potassium has a greater or lesser effect on blood pressure compared with potassium chloride. We performed a randomized crossover trial comparing potassium chloride with potassium citrate (96 mmol/d, each for 1 week) in 14 hypertensive individuals. At baseline, blood pressure was 151+/-16/93+/-7 mm Hg with a 24-hour urinary potassium of 81+/-24 mmol. During the randomized crossover part of the study, blood pressure was 140+/-12/88+/-7 mm Hg with potassium chloride (24-hour urinary potassium: 164+/-36 mmol) and 138+/-12/88+/-6 mm Hg with potassium citrate (24-hour urinary potassium: 160+/-33 mmol). These blood pressures were significantly lower compared with that at baseline; however, there was no significant difference in blood pressure between potassium chloride and potassium citrate, mean difference (95% confidence interval): 1.6 (-2.3 to 5.6) mm Hg for systolic and 0.6 (-2.4 to 3.7) mm Hg for diastolic. Our results, in conjunction with the evidence from many previous trials that potassium chloride has a significant blood pressure-lowering effect, suggest that potassium citrate has a similar effect on blood pressure as potassium chloride. These results support other evidence for an increase in potassium intake and indicate that potassium does not need to be given in the form of chloride to lower blood pressure. Increasing the consumption of foods high in potassium is likely to have the same effect on blood pressure as potassium chloride.

Adult↗
PubMed1986

Paradoxical potassium depletion: a renal mechanism for extrarenal potassium adaptation.

Following nephrectomy and acute potassium loading, animals previously maintained on a high potassium diet have a smaller increment in plasma potassium than do animals on a control diet. The mechanism of this "extrarenal potassium adaptation" is not known. To explore the role of potassium depletion in this process, we studied rats adapted to either a high potassium (HK) or control (C) diet. When dietary potassium was withdrawn, urinary potassium losses in HK rats greatly exceeded those in C rats for at least two days, leading to greater potassium depletion in HK than C animals. A smaller increment in plasma potassium in HK compared to C rats was seen only after prolonged fasting preceded nephrectomy and acute potassium loading. Correction of potassium depletion incurred during fasting abolished extrarenal potassium adaptation. We conclude: after withdrawal of dietary potassium, urinary potassium losses are much greater in HK than in C rats; if the duration of dietary potassium deprivation is sufficient, these urinary potassium losses will cause potassium-adapted animals to paradoxically become more potassium depleted than controls; and this paradoxical potassium depletion may be responsible for extrarenal potassium adaptation.

Adaptation, Physiological↗
PubMed1991

Bioavailability of potassium and magnesium, and citraturic response from potassium-magnesium citrate.

The bioavailability of potassium and magnesium, and the citraturic response were determined for the new compound, potassium-magnesium citrate, in 14 normal volunteers. Results were compared to those of potassium citrate and magnesium citrate. Each subject participated in 4 phases of study: potassium-magnesium citrate, potassium citrate, magnesium citrate and potassium chloride. After stabilization on a metabolic diet, each subject ingested a single load of a test medication followed by timed urine collections for the next 24 hours. Test loads included potassium-magnesium citrate (49 mEq. potassium, 24.5 mEq. magnesium and 73.5 mEq. citrate), potassium citrate (50 mEq.), potassium chloride (50 mEq.) and magnesium citrate (25 mEq.) Urinary potassium, magnesium and citrate were measured for each collection period. Potassium-magnesium citrate provided an equivalent potassium bioavailability as potassium citrate and potassium chloride, and a comparable magnesium bioavailability as magnesium citrate. However, it gave the highest citraturic response, since the cumulative increment in urinary citrate post-load was 129 mg. daily for potassium-magnesium citrate, 105 mg. daily for potassium citrate and 35 mg. daily for magnesium citrate. Thus, potassium-magnesium citrate gave an optimum citraturic response in addition to providing absorbable potassium and magnesium.

Adult↗
PubMed1985

Role of aldosterone and dietary potassium in potassium adaptation in the distal colon of the rat.

The present experiments were designed to differentiate the effects of aldosterone and chronic potassium loading in the mechanism of colonic potassium adaptation, using a recently described animal model that permits systematic manipulation of aldosterone and dietary potassium. Unidirectional 42K fluxes were performed under short-circuit conditions across isolated distal colonic mucosa from rats with intact adrenal glands and in adrenalectomized, hormone-replaced animals. Administration of a potassium-enriched diet reversed net potassium absorption (+0.43 +/- 0.10 muEq/h.cm2) in intact animals to net potassium secretion (-0.76 +/- 0.08 muEq/h.cm2). Infusion of aldosterone in adrenalectomized animals, in an amount equivalent to that produced by potassium loading in intact rats, reduced JnetK to zero (-0.03 +/- 0.06 muEq/h.cm2). Similarly, zero net potassium transport (-0.14 +/- 0.08 muEq/h.cm2) was observed when experimental rats were fed a potassium-enriched diet and maintained with basal aldosterone levels. Therefore, both elevated aldosterone levels and a potassium-enriched diet had an effect on net potassium transport, but neither produced the full effects of chronic potassium loading. An increase in net potassium secretion (-0.57 +/- 0.07 myEq/h.cm2) comparable to that of intact potassium-loaded animals did, however, occur when potassium loading and elevated aldosterone levels were combined in experimental animals. These studies demonstrate that (a) chronic potassium loading alters active potassium transport by an aldosterone-independent mechanism and (b) the mechanism of chronic potassium adaptation represents the additive effects of increased dietary potassium and aldosterone.

Adaptation, Physiological↗
PubMed1998

Potassium diet as a determinant for the renal response to systemic potassium channel modulation in anesthetized rats.

The role of potassium intake in the response of kidney function and plasma renin activity (PRA) to systemic application of U37883A (4-morpholinecarboximidine-N-1-adamantyl-N'-cyclohexyl-hydro chloride), a putative blocker of ATP-sensitive potassium channels (K(ATP)), and P1075 (N-cyano-N'-(1,1-dimethylpropyl)-N"-pyridylguanidine), an opener of K(ATP) channels, was studied in the anesthetized rat. It was found that under normal potassium diet (0.7% K), U37883A (15 mg/kg, i.v.) increased urinary flow rate (UV) and sodium excretion (UNaV), decreased urinary potassium excretion (UKV), and significantly diminished heart rate (HR) without affecting mean arterial blood pressure (MAP) or glomerular filtration rate (GFR). P1075 (10 microg/kg, i.v.) lowered UV, UNaV and UKV, at least in part due to the fall in MAP and GFR. PRA was diminished by U37883A and increased by P1075. Variation in potassium diet (0.04 or 2% K) left the response in MAP, HR or GFR to both potassium channel modulators essentially unchanged. The reduction in renal excretion rates to P1075 also appeared unaffected, further supporting a predominant role of the change in MAP and GFR in this response. Variation in potassium diet, however, elicited the following alterations: (1) under both low and high potassium diet U37883A did no longer cause a significant natriuresis; (2) U37883A elicited a significant kaliuresis under high potassium diet, whereas potassium excretion remained essentially unchanged on very low levels under low potassium diet; (3) the increase in PRA to P1075 was blunted under low potassium diet. Additional experiments provided evidence that P1075 releases renin from freshly isolated juxtaglomerular cells of rats on normal but not on low potassium diet. In summary, systemic potassium channel modulation employing U37883A or P1075, respectively, exerts distinct effects on blood pressure and heart rate independent of potassium diet. In contrast, potassium diet appears to be a determinant for the concomitant responses in plasma renin activity and renal sodium and potassium excretion.

Adamantane↗
PubMed1981

Role of the medullary collecting duct in potassium excretion in potassium-adapted animals.

Previous studies have demonstrated that the rate of urinary potassium excretion is markedly greater in animals fed a high potassium diet than in animals on a control diet before and during the acute infusion of potassium salts. Because the contribution of the medullary collecting duct to urinary potassium under these conditions has not been determined, microcatheterization studies were performed to elucidate the role of that nephron segment in regulating potassium excretion in controls and in animals on a potassium-enriched diet. Although there was no evidence of net transport of potassium by the medullary collecting duct in control animals under basal conditions, net secretion of potassium by that nephron segment accounted for nearly one half of the increased rate of urinary excretion in animals fed a high potassium diet. During acute infusion of potassium salts, potassium secretion by the medullary portion of the collecting duct contributed approximately one half of the potassium in the final urine samples in both controls and animals fed a high potassium diet. Because the rate of urinary excretion was twofold greater in experimental animals during acute potassium loading, absolute potassium secretion in medullary collecting duct was twice the control rate in animals adapted to a high potassium dietary intake. These data demonstrate, therefore, that the medullary collecting duct plays an important role in regulating the excretion of potassium when the excretory load is either acutely or chronically increased.

Animals↗
PubMed1988

Reduced concentrations of potassium, magnesium, and sodium-potassium pumps in human skeletal muscle during treatment with diuretics.

Animal studies have shown that potassium depletion induced by diuretics or potassium deficient fodder leads to a selective decrease in the concentrations of potassium and in the concentration of sodium-potassium pumps in skeletal muscle. In 25 patients who had received diuretics for 2-14 years the mean concentrations of potassium, magnesium, and sodium-potassium pumps were measured in skeletal muscle biopsy specimens and were significantly lower than in those from a group of age matched controls. The reductions in all three variables were significant in those patients receiving diuretics for arterial hypertension as well as in those being treated for congestive heart failure. In 14 patients the mean muscle potassium concentration was below the control range, but only one of those was hypokalaemic (3.4 mmol/l), and 13 were receiving potassium supplements. In 15 patients the mean muscle magnesium concentration was below normal, and the mean muscle potassium and magnesium concentrations showed a linear correlation. In 12 patients in whom the mean muscle potassium concentration was below 80 mumol/g wet weight there was a linear correlation between the cellular potassium:sodium ratio and the concentration of 3H-ouabain binding sites indicating that potassium deficiency also leads to a down regulation of sodium-potassium pumps in human skeletal muscle. In spite of potassium supplements long term treatment with diuretics may lead to potassium and magnesium deficiencies, which are not detectable using the standard methods of serum analysis. The changes in concentrations of electrolytes and sodium-potassium pumps associated with treatment with diuretics may impair muscle function and potassium homoeostasis and interfere with the distribution of digitalis glycosides.

Adult↗
PubMed1976

Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. II. Effects of different medium potassium concentrations on epithelial cell composition.

Epithelial cells from hemibladders incubated in potassium-free sodium Ringer's serosal medium lost potassium, both in exchange for serosal sodium and with chloride and water. Cellular sodium of mucosal origin did not change. The loss of cellular potassium, chloride and water closely followed the fall in short-circuit current (SCC). One third as much potassium, chloride and water were lost in 1 mM potassium serosal medium; SCC fell 1/3 as much. Potassium-free choline Ringer's serosal medium abolished the initial increase in SCC and reduced the fall in cellular potassiu, chloride and water and in SCC. Ouabain (10(-2)M) in potassium-free medium prevented the initial increase in SCC and the loss of cellular chloride and water. Ouabain (5 X 10(-4)M) caused loss of cellular potassium in exchange for mucosal and serosal sodium, effects different from those of absence of serosal potassium although SCC was similarly inhibited. Sodium-free mucosal medium abolished SCC and prevented the initial transient of SCC and diminished loss of cellular potassium, chloride and water on removing serosal potassium. When serosal potassium concentration was increased considerably, cells gained potassium, chloride and water, and in 116 mM potassium media, lost sodium of serosal origin. A hypothesis is advanced to explain the transients in SCC on changing serosal potassium concentration. The fall in cellular potassium, not water, probably inhibits sodium transport in media of less than 2 mM potassium.

Animals↗
PubMed1976

Relationships between serosal medium potassium concentration and sodium transport in toad urinary bladder. III. Exchangeability of epithelial cellular potassium.

The exchangeability of toad bladder epithelial cell potassium has been investigated. An insignificant amount of cellular potassium exchanged with mucosal medium 42K. From the rate of uptake of 42K into the cells from the serosal medium at least two cellular potassium pools were identified. The more rapidly exchanging pool contained about one-quarter to one-third of the cellular potassium and exchanged with a half-time of about 30 min. It was from this pool that potassium was lost from cells exposed to ouabain or to a potassium-free medium. In addition, when 3.5 mM rubidium replaced 3.5 mM potassium in sodium Ringer's the epithelial cells lost in 60 min about one-quarter of their cellular potassium in exchange for rubidium. Inhibition of transepithelial sodium transport by amiloride, 10(-5) mM, seemed to depress the rate of potassium uptake into the more rapidly exchanging pool without affecting total cellular potassium content. However, stimulation of transepithelial sodium transport by vasopressin appeared not to affect the rate of potassium uptake. The rate of potassium uptake into this pool seemed much less than that required for a tight 1:1 coupling between transepithelial sodium transport and potassium uptake. The remaining cellular potassium exchanged at a much slower rate and even after 19 hours of incubation only 67% of cellular potassium was labelled. If this slower exchanging potassium represents a single pool, 99% of cellular potassium would be labelled only after incubation with 42K for 56 hours.

Animals↗
PubMed1990

The effect of dietary sodium and potassium intake on potassium secretion and kinetics in rat distal colon.

1. Potassium secretion by the distal colon was examined in relation to the secretion of chloride and absorption of sodium and to the epithelial turnover of 86Rb+ (as an analogue of potassium) in vivo in rats fed a standard, a potassium-rich or a sodium-depleted diet. 2. An acute intravenous potassium load stimulated potassium secretion two- to threefold. In rats fed the standard diet, sodium secretion was also increased but no significant change in the lumen-to-plasma sodium flux was detected. The potassium and sodium secretions were accompanied by increased chloride secretion which occurred even when the intravenous load contained no chloride. In rats fed the potassium-rich diet, there was a small increase in sodium absorption and a less marked increased of chloride secretion. In the sodium-depleted rats, however, about 70-80% of the increased potassium secretion was balanced by increased sodium absorption. 3. The epithelial turnover rate of 86Rb+ in the rats fed the potassium-rich (t1/2 12-14 min) and the sodium-depleted (t1/2 11-13 min) diets was faster than that of those of the standard diet (t1/2 22-27 min). 4. The epithelial potassium content was 304 +/- 9 nmol (mg dry weight)-1 and was not significantly altered despite considerable variations in potassium secretion rate induced by dietary changes and acute potassium loading. 5. It is concluded that epithelial potassium turnover rate is increased during chronic states of increased potassium secretion and that the rise in potassium secretion is consistent with increased activity of the basolateral Na(+)-K+ pump. Whether the increased potassium secretion is associated with chloride secretion or with increased sodium absorption appears to depend on the absence or presence of the amiloride-sensitive sodium pathway in the apical membrane.

Amiloride↗
PubMed1975

Total body potassium measurements in 230 patients. A study of potassium depletion.

Three groups of patients with suspected potassium depletion were studied. Twenty-nine obese patients were observed before and up to 1 year after an intestinal shunt operation. During the first week after operation they lost almost 3 grams of potassium per day. The percentage potassium loss was much larger than the percentage weight loss. A significant decrease of serum potassium was also noted during the first week after operation. In contrast to the total body potassium, however, the serum potassium remained within normal limits in all patients except two. Fourteen patients subjected to a cardiac operation also showed a significant decrease of total body potassium concentration 1 week after operation. The serum potassium remained within normal limits. In 187 patients with suspected potassium depletion the total body potassium had been measured, and the results were examined retrospectively. In 38 of these patients the measured total body potassium was outside a 94% confidence interval for an individually predicted value, even though 26 of these 38 patients were taking oral potassium chloride tablets. In 23 of these 38 patients two or three risk factors - hypoalbumin-emia, treatment with diuretics, and treatment with digitalis - were present simultaneously, and in 10 patients one factor was present. Only 8 of the 38 patients had a low serum potassium value. It may therefore be concluded that the total body potassium measurement, when compared with an individually predicted value, seems to be more sensitive in estimation of potassium depletion than the commonly used serum potassium method.

Adipose Tissue↗
PubMed2004

Changes in erythrocyte contents of potassium, sodium and magnesium and Na, K-pump activity after the administration of potassium and magnesium salts.

Low potassium and magnesium status and decreased Na, K-pump activity is an endemic condition among rural Northeast Thais. The authors examined the effect of supplementing potassium and magnesium on erythrocyte potassium, sodium and magnesium content and on Na, K-pump activity. Rural Northeast Thai renal stone patients (62) were recruited, divided into four groups and supplemented for one month with potassium chloride (Group1, n = 16), potassium-sodium citrate (Group2, n = 15), chelated magnesium (Group 3, n =16) and potassium-magnesium citrate (Group 4, n =15) in order to achieve 40 mmol potassium, 10 mmol magnesium and 60 mmol citrate daily. After supplementation with potassium (Groups 1, 2 and 4), plasma potassium and Na, K-pump activity rose significantly in Groups 1, 2 and 4, but erythrocyte potassium rose only in Groups 2 and 4. When supplementing elemental magnesium (Groups 3 and 4), the chelated magnesium caused a significant increase in plasma potassium, erythrocyte potassium, sodium and magnesium without a significant increase in Na, K-pump activity. By contrast, potassium-magnesium citrate caused a significant increase in erythrocyte potassium and magnesium and Na, K-pump activity, but depressed erythrocyte sodium. These results suggest the forms of potassium and /or magnesium salts being supplemented should be considered because they affect erythrocyte potassium, sodium and magnesium content and Na, K-pump activity differently.

Erythrocytes↗
PubMed1999

Potassium secretion in rat distal colon during dietary potassium loading: role of pH regulated apical potassium channels.

BACKGROUND: Chronic dietary K+ loading increases the abundance of large conductance (210 pS) apical K+ channels in surface cells of rat distal colon, resulting in enhanced K+ secretion in this epithelium. However, the factors involved in the regulation of these K+ channels are at present unclear. AIMS: To evaluate the effect of dietary K+ loading on intracellular pH and its relation to large conductance apical K+ channel activity in surface cells of rat distal colon. METHODS/RESULTS: As assessed by fluorescent imaging, intracellular pH was higher in K+ loaded animals (7.48 (0.09)) than in controls (7.07 (0.04); p<0.01) when surface cells were bathed in NaCl solution, and a similar difference in intracellular pH was observed when cells were bathed in Na2SO4 solution (7.67 (0.09) and 6.92 (0.05) respectively; p<0.001). Ethylisopropylamiloride (EIPA; an inhibitor of Na+-H+ exchange; 1 microM) decreased intracellular pH when surface cells from K+ loaded animals were bathed in either solution, although the decrease was greater when the solution contained NaCl (DeltapH 0.50 (0.03)) rather than Na2SO4 (DeltapH 0. 18 (0.02); p<0.05). In contrast, EIPA had no effect in cells from control animals. As assessed by patch clamp recording techniques, the activity of large conductance K+ channels in excised inside-out membrane patches from distal colonic surface cells of K+ loaded animals increased twofold when the bath pH was raised from 7.40 to 7. 60. As assessed by cell attached patches in distal colonic surface cells from K+ loaded animals, the addition of 1 M EIPA decreased K+ channel activity by 50%, consistent with reversal of Na+-H+ exchange mediated intracellular alkalinisation. CONCLUSION: Intracellular alkalinisation stimulates pH sensitive large conductance apical K+ channels in rat distal colonic surface cells as part of the K+ secretory response to chronic dietary K+ loading. Intracellular alkalinisation seems to reflect an increase in EIPA sensitive Na+-H+ exchange, which may be a manifestation of the secondary hyperaldosteronism associated with this model of colonic K+ adaptation.

Amiloride↗