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PubMed1976

The effect of high rates of vasopressin administration on renal potassium and sodium excretion during potassium loading in the sheep.

1 The influence of potassium loading on the renal excretion of sodium, potassium and solute during high rate vasopressin administration has been investigated in sheep. 2 Adrenalectomized sheep were infused with 0.43 M KCl at 2 ml/min for 2-2.5 hours. Coincident with the rise in plasma potassium concentration, the urinary excretion of sodium, potassium, solute and water was increased as was the reabsorption of solute-free water. The rates of urinary excretion of sodium and potassium, osmolal clearance (COsm) and solute-free water reabsorption (TcH2O) for the first 50 min of potassium infusion were each found to be linearly related to the plasma potassium concentration. 3 After 50 min an infusion of vasopressin at 1 or 4 mu/min was superimposed on the potassium infusion for a period of 30 minutes. The administration of vasopressin was consistently associated with further augmentation of potassium excretion and clearance, of osmolal clearance and of solute-free water reabsorption to values above those anticipated from the pre-vasopressin regression lines for these parameters. Urinary sodium showed a coincident depression in the rate of excretion and clearance during the same period. 4 Thirty to fifty minutes after the cessation of vasopressin infusion the potassium and sodium excretions had returnied to values which approximated the pre-vasopressin relations between plasma potassium and the urinary excretions of these ions. 5 Both rates of vasopressin infusion were equally effective in increasing the potassium clearance. Any differences in clearance between the two rates of vasopressin administration were not statistically significant. 6 The large increments in potassium excretion (averaging greater than 40%) were interpreted as indicating that, when vasopressin is present at high concentrations, the distal tubule is one site of action of the hormone in the nephron of sheep.

Animals↗
PubMed1983

Interrelated effects of aldosterone and plasma potassium on potassium excretion.

The interacting effects of aldosterone and plasma potassium concentration on steady-state renal potassium excretion were studied in two groups of chronically adrenalectomized dogs. In group I (six dogs, 22.9 kg) aldosterone was infused intravenously at 20 micrograms/day while potassium intake was changed in steps of 7-10 days duration from 10 to 30 to 100 meq/day. At the completion of each step, plasma potassium concentration, urinary potassium excretion, and other variables that potentially may affect renal function were measured. In group II (six dogs, 22.2 kg) a similar protocol was followed except that aldosterone was infused at 250 micrograms/day and the potassium intake levels were 30, 100, and 200 meq/day. Plasma potassium concentration and excretion data for the 20 micrograms/day group were: 3.22 +/- 0.26 meq/liter and 5 +/- 1 meq/day, 4.35 +/- 0.08 meq/liter and 21 +/- 2 meq/day, and 5.88 meq/liter and 82 +/- 3 meq/day at the 10, 30, and 100 meq/day intake levels, respectively. For the 250 micrograms/day group the values were: 2.72 +/- 0.18 meq/liter and 28 +/- 7 meq/day, 4.16 +/- 0.14 meq/liter and 71 +/- 8 meq/day, and 4.40 +/- 0.14 meq/liter and 172 +/- 26 meq/day at the 30, 100, and 200 meq/day intake levels. Therefore, the increase in aldosterone infusion rate shifted the relationship between plasma potassium concentration and potassium excretion to the left so that at a given level of plasma potassium a greater amount of potassium was excreted. In the normal range of plasma potassium concentration (4.00-4.40 meq/liter) the increase in aldosterone levels resulted in a four- to eightfold increase in daily potassium excretion.

Aldosterone↗
PubMed1990

Potassium-39 nuclear magnetic resonance observation of intracellular potassium without chemical shift reagents during metabolic inhibition in the isolated perfused rat heart.

The intracellular potassium content of perfused rat heart was measured by potassium-39 nuclear magnetic resonance (NMR) spectroscopy at 33 degrees C with an inversion recovery technique based on the fact that the spin-lattice relaxation time (T1) of the intracellular potassium (8.3 msec at 8.45 T) is much faster than that of the extracellular potassium (68 msec). Intracellular potassium decreased to 60.2 +/- 4.3% of the control level (mean +/- SEM, n = 6) at 40 minutes from the start of metabolic inhibition (2 mM cyanide, 0 mM glucose). Removal of cyanide restored intracellular potassium to 94.2 +/- 3.9% at 30 minutes from the restart of oxidative metabolism. The cumulative potassium loss was determined from the flow rate and potassium concentration of the coronary effluent, which reached 139 +/- 12 mumol/g dry wt during 40 minutes of metabolic inhibition. This value was calculated as 41.8% of intracellular potassium in the control heart and agreed with the decrement of intracellular potassium measured by NMR. During the metabolic inhibition and recovery period, a linear correlation was observed between the changes in 39K NMR-observed intracellular potassium and the cumulative potassium loss. The present results evaluate the inversion recovery technique as a method to successfully monitor the myocardial intracellular potassium.

Animals↗
PubMed2000

Basolateral K-Cl cotransporter regulates colonic potassium absorption in potassium depletion.

Active potassium absorption in the rat distal colon is electroneutral, Na(+)-independent, partially chloride-dependent, and energized by an apical membrane H,K-ATPase. Both dietary sodium and dietary potassium depletion substantially increase active potassium absorption. We have recently reported that sodium depletion up-regulates H,K-ATPase alpha-subunit mRNA and protein expression, whereas potassium depletion up-regulates H,K-ATPase beta-subunit mRNA and protein expression. Because overall potassium absorption is non-conductive, K-Cl cotransport (KCC) at the basolateral membrane may also be involved in potassium absorption. Although KCC1 has not been cloned from the colon, we established, in Northern blot analysis with mRNA from the rat distal colon using rabbit kidney KCC1 cDNA as a probe, the presence of an expected size mRNA in the rat colon. This KCC1 mRNA is substantially increased by potassium depletion but only minimally by sodium depletion. KCC1-specific antibody identified a 155-kDa protein in rat colonic basolateral membrane. Potassium depletion but not sodium depletion resulted in an increase in KCC1 protein expression in basolateral membrane. The increase of colonic KCC1 mRNA abundance and KCC1 protein expression in potassium depletion of the rat colonic basolateral membrane suggests that K-Cl cotransporter: 1) is involved in transepithelial potassium absorption and 2) regulates the increase in potassium absorption induced by dietary potassium depletion. We conclude that active potassium absorption in the rat distal colon involves the coordinated regulation of both apical membrane H,K-ATPase and basolateral membrane KCC1 protein.

Animals↗
PubMed1987

Potassium influx into maize root systems : influence of root potassium concentration and ambient ammonium.

Potassium influx into roots of dark-grown decapitated maize seedling (Zea mays L., cv Pioneer 3369A) was examined in presence and absence of ambient ammonium and at various root potassium concentrations. Six-day old seedlings which were dependent on the endosperm reserves for their energy source were exposed to KCl (labeled with (86)Rb) ranging from 5 to 200 micromolar. At both low (13 micromoles per gram fresh weight) and high (100 micromoles per gram fresh weight) root potassium concentration, isotherms indicated two potassium influx systems, one approaching saturation at 50 to 100 micromolar potassium and an additional one tentatively considered to be linear. A mixed-type inhibition by ammonium for the low-concentration saturable system was indicated by a concomitant decrease in V(max) and increase in K(m). High root potassium concentration decreased V(max) but had little effect on K(m) of this system. The rate constant for the second quasilinear system was decreased by ambient ammonium and by high root potassium status. Transfer of high potassium roots to potassium-free solutions resulted in an increase in influx within 2 hours; by 24 hours influx significantly exceeded that of roots not previously exposed to potassium. In roots of both low and high root potassium concentrations, potassium influx was restricted progressively as ambient ammonium increased to about 100 micromolar, but there was little further inhibition as ammonium concentrations increased beyond that to 500 micromolar. The data imply that potassium influx has two components, one subject to inhibition by ambient ammonium and one relatively resistant.

Journal Article↗
PubMed1981

Intracellular and exchangeable potassium in cirrhosis. Evidence against the occurrence of potassium depletion in cirrhosis with ascites.

The intracellular potassium content of leukocytes, the extracellular fluid volume (82Br space), and exchangeable potassium were determined in 28 patients with cirrhosis of the liver (18 with ascites) and in 15 hospitalized controls. No intracellular potassium depletion could be identified in these patients. Leukocyte potassium was similar in cirrhotic patients with and without ascites (355.9 +/- 25.3 and 348.1 +/- 31.9 mEq/kg of dry solids, respectively) and in hospitalized controls (359.7 +/- 27.4) (mean +/- SD). The extracellular fluid volume was similar in controls and cirrhotics without ascites, but markedly increased in cirrhotics with ascites. The exchangeable potassium (mEq/kg of body weight) was similar in nonascitic cirrhotics and in hospitalized controls, but significantly lower in patients with cirrhosis and ascites. However, when the estimated weight of the extracellular fluid volume was substrated from the total body weight, thus obviating the influence of the increased extracellular fluid volume of ascitic patients in the body weight, the exchangeable potassium (mEq/kg of "corrected" body weight) was similar in cirrhosis with ascites (52.9 +/- 6.7 mEq/kg), nonascitic cirrhotics (55.8 +/- 6.1 mEq/kg) and hospitalized controls (55.0 +/- 8.3 mEq/kg), and a significant correlation was obtained between the exchangeable potassium and the leukocyte potassium content. In five patients, the measurements were repeated after relieving ascites with diuretics. No change was observed in the leukocyte potassium, but exchangeable potassium (mEq/kg of body weight) increased, reaching values not significantly different from controls or nonascitic cirrhotics. The exchangeable potassium (mEq/kg of "correct" body weight) did not change. Our results strongly suggest that potassium depletion was not present in the series of cirrhotic patients studied.

Aged↗
PubMed1999

Expression of adenosine triphosphate-sensitive potassium channel subunits in female rat reproductive tissues: overlapping distribution of messenger ribonucleic acid for weak inwardly rectifying potassium channel subunit 6.1 and sulfonylurea-binding regulatory subunit 2.

OBJECTIVE: Potassium channel activation has been shown to decrease uterine tone and is a target for inhibition of uterine activity in the treatment of preterm labor. In addition, potassium channel activation also appears to be involved in oocyte maturation. The specific potassium channels responsible for these channel currents have not been identified but are known to be responsive to such agents as pinacidil and to be inhibited by glibenclamide. These findings suggest the presence of an adenosine triphosphate-sensitive potassium channel that is a complex of a weak inwardly rectifying potassium channel subunit 6.1 or 6.2 and sulfonylurea-binding regulatory subunit 1 or 2. STUDY DESIGN: The technique of reverse transcriptase-polymerase chain reaction was used to detect the presence of messenger ribonucleic acid for sulfonylurea-binding regulatory subunit 1 and 2 and weak inwardly rectifying potassium channel subunit 6.1 and 6.2 in the ovary and myometrium of the pregnant rat. In situ hybridization histochemical analysis was used to identify the specific cell types expressing each messenger ribonucleic acid. RESULTS: Reverse transcriptase-polymerase chain reaction analysis found expression of messenger ribonucleic acid for sulfonylurea-binding regulatory subunits 1 and 2B and messenger ribonucleic acid for weak inwardly rectifying potassium channel subunit 6.1 in rat myometrium and ovary during gestation. There was no evidence for expression of weak inwardly rectifying potassium channel subunit 6.2 messenger ribonucleic acid in the ovary or the myometrium of the pregnant rat. In situ hybridization histochemical examination localized expression of messenger ribonucleic acid for sulfonylurea-binding regulatory subunit 2B and messenger ribonucleic acid for weak inwardly rectifying potassium channel subunit 6.1 to uterine myocytes and granulosa cells of the corpus luteum. The cells expressing sulfonylurea-binding regulatory subunit 1 messenger ribonucleic acid could not be identified because of the scarcity of this messenger ribonucleic acid. Messenger ribonucleic acid for sulfonylurea-binding regulatory subunit 1, messenger ribonucleic acid for sulfonylurea-binding regulatory subunit 2B, and messenger ribonucleic acid for weak inwardly rectifying potassium channel subunit 6.1 were also observed in the placenta by in situ hybridization histochemical examination. CONCLUSION: The results suggest that the major adenosine triphosphate-sensitive potassium channel expressed in the myometrium and the corpus luteum during pregnancy is a complex of sulfonylurea-binding regulatory subunit 2B and weak inwardly rectifying potassium channel subunit 6.1.

ATP-Binding Cassette Transporters↗
PubMed1979

Suppression of potassium-recycling in the renal medulla by short-term potassium deprivation.

Recently we proposed that potassium, like urea, normally undergoes medullary recycling from collecting tubule to the pars recta or descending limb of the juxtamedullary nephron and suggested that the extent of recycling is a function of the concentration of potassium in collecting tubule fluid. To test this hypothesis further, we fed young rats a potassium-free diet for 3 days and then prepared them for micropuncture of the left renal papilla. Compared to findings in normally fed animals, potassium deprivation caused a significant fall in plasma potassium and urinary excretion of potassium. There was a striking decrease in the fraction of filtered potassium remaining at the end of the justamedullary descending limb for 94 +/- 11% to 38 +/- 3% (P less than 0.001). The latter value is not significantly different from the fraction of filtered sodium remaining (36 +/- 4%) and suggests that net addition of potassium to the pars recta or descending limb was completely abolished. A correlation was observed between the fraction of filtered potassium remaining at the end of the descending limb and either urinary potassium excretion (P less than 0.001) or urinary potassium concentration(P less than 0.001) in the contralateral unexposed kidney. These results lend further support to the hypothesis of medullary recycling of potassium.

Animals↗
PubMed1975

Influence of glycosides on myocardial potassium and sodium concentration in acute and chronic potassium deficiency.

The analytical assay of intracellular potassium ([Ki]) and sodium ([Nai]) concentration of guinea pig papillary muscle measured in in vitro experiments shows that: 1) 5 X 10(-7) M g-strophanthin causes a decrease of [Ki] under control conditions, in acute as well as in chronic potassium deficiency, 2) a more marked glycoside effect is seen when the extracellular potassium concentration is reduced from 4.7 to 2mEq/1; this finding, therefore, is in good agreement with the observation that glucoside binding to its receptor at the cellular membrane is enhanced when potassium concentration is decreased, 3) whereas in chronic potassium deficiency normal [Ki] and [Nai] are maintained, acute potassium deficiency is accompanied by a loss of cellular K and gain of cellular Na. Under the influence of cardioactive glycosides, in chronic potassium depletion higher intracellular potassium and lower intracellular sodium concentrations are maintained than in acute potassium depletion. It is supposed tha t the net changes which are caused by a reduction of [Ke] in acute potassium deficiency in contrast to chronical potassium deficiency predispose to glycoside toxicity. These changes may therefore be the cause of the clinical observation that acute hypokalemia is associated with a greater glycoside sensitivity than chronic potassium deficiency.

Acute Disease↗
PubMed1985

Effect of potassium depletion on acidosis-induced changes in plasma potassium concentration.

It is unknown whether acute metabolic acidosis causes increases in plasma potassium concentration despite pre-existing potassium depletion. In fact, it has long been assumed clinically that acidosis-induced acute hyperkalemia may be masked by potassium depletion. In order to assess this question, moderate to severe potassium depletion was produced in 7 female mongrel dogs (potassium-depleted group) over a 12-day period with injections of desoxycorticosterone acetate (DOCA), NaCl added to the drinking water, and a potassium-free diet. Six dogs (control group) received regular chow, identical NaCl supplements, and sham injections of DOCA. The achievement of potassium depletion was documented by significant differences between the two groups in urinary potassium and in muscle and plasma potassium levels (potassium-depleted group: 0.9 +/- 0.2 mEq/24 h, 19 +/- 3 mEq/100 g dry weight, 1.9 +/- 0.1 mEq/1; control group: 44 +/- 11 mEq/24 h [p less than 0.025], 30 +/- 1 mEq/100 g [p less than 0.005], 3.5 +/- 0.1 mEq/l [p less than 0.005]). There were no statistically significant differences between the groups in blood pH or [HCO3]. On day 13, an NH4Cl acid-load was given (5 mEq/kg body weight i.v. over 3 h in 0.45% NaCl using pentobarbital anesthesia). Following acid-loading, the increases in plasma [K] were significantly greater in the control group than in the potassium-depleted group only at 90 and 120 min. There were no significant differences in the maximal increases from baseline in plasma [K] (potassium-depleted group: 0.6 +/- 0.1 mEq/l, 31 +/- 6%; control group: 1.5 +/- 0.4 mEq/l, 41 +/- 10%).(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗