scholarly journals Effects of potassium depletion on renal tubular chloride transport in the rat

1978 ◽  
Vol 14 (5) ◽  
pp. 414-427 ◽  
Author(s):  
Robert G. Luke ◽  
Fred S. Wright ◽  
Nicole Fowler ◽  
Michael Kashgarian ◽  
Gerhard H. Giebisch
Keyword(s):  
Chloride Transport ◽  
Potassium Depletion ◽  
Renal Tubular

Defect in the Renal Tubular Reabsorption of Water Associated With Potassium Depletion in Rats

1957 ◽  
Vol 189 (3) ◽  
pp. 557-563 ◽  
Author(s):  
Walter Hollander ◽  
Robert W. Winters ◽  
T. Franklin Williams ◽  
John Bradley ◽  
Jean Oliver ◽  
...  
Keyword(s):  
Urinary Concentration ◽  
Potassium Depletion ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Renal Tubular Reabsorption ◽  
Renal Concentrating Mechanism ◽  
Renal Tubular ◽  
Relationship Of ◽  
The Relationship ◽  
K Depletion

The effect of graded degrees of K depletion on the ability to produce a concentrated urine was studied in Sprague-Dawley rats. With increasing degrees of K depletion, as measured by the concentration of K in fat-free skeletal muscle, there was a progrossive decrease in the maximum urinary concentration. This defect of the renal concentrating mechanism appeared to be better correlated with the degree than with the duration of potassium depletion and could be demonstrated either by the use of exogenous vasopressin or by water deprivation. The potassium-deficient rats in at least one experiment developed a significant polydipsia. The data do not allow any conclusions with respect to the relationship of the polydipsia to the renal concentrating defect except that the latter at least was not severe at the onset of the increased water intake.

Micropuncture study of proximal renal tubular chloride transport during hypercapnea in the rat

1965 ◽  
Vol 209 (3) ◽  
pp. 655-658 ◽  
Author(s):  
Michael Kashgarian ◽  
Yves Warren ◽  
Howard Levitin
Keyword(s):  
Chloride Transport ◽  
Electrical Potential ◽  
Stopped Flow ◽  
Electrical Potential Difference ◽  
Micropuncture Study ◽  
Tubular Lumen ◽  
Proximal Tubular ◽  
Renal Tubular ◽  
Electrochemical Equilibrium ◽  
Anion Pump

The electrical potential difference and the concentration of chloride in tubular fluid and plasma were measured in stopped-flow microperfusion of the proximal tubule of rats breathing either air or 12% CO2 in air. Perfusion with 10% PVP completely stopped net transtubular fluid movement. Chloride was not in electrochemical equilibrium under these conditions and hypercapnea increased the concentration of chloride in tubular fluid relative to that in plasma. This suggests that the net reabsorption of chloride must overcome a force which moves chloride into the tubular lumen. An anion pump is postulated which secretes chloride into the tubular lumen and is linked to acidification of proximal tubular fluid.

Effects of potassium depletion on renal tubular sodium and water reabsorption in the dog

1972 ◽  
Vol 222 (4) ◽  
pp. 928-937 ◽  
Author(s):  
B Rosenbaum ◽  
MJ Kinney ◽  
FC Scudder ◽  
VA DiScala ◽  
RM Stein
Keyword(s):  
Potassium Depletion ◽  
Water Reabsorption ◽  
Renal Tubular

Renal Tubular Acidosis in a Patient with Recurrent Metabolic Alkalosis

PEDIATRICS ◽  
1983 ◽  
Vol 72 (2) ◽  
pp. 207-210
Author(s):  
Leonard C. Hymes ◽  
Barry L. Warshaw
Keyword(s):  
Renal Tubular Acidosis ◽  
Serum Potassium ◽  
Metabolic Alkalosis ◽  
Failure To Thrive ◽  
Unusual Presentation ◽  
Potassium Depletion ◽  
Type I ◽  
Serum Bicarbonate ◽  
Urine Ph ◽  
Renal Tubular

A 7-month-old infant with failure to thrive and recurrent episodes of vomiting and metabolic alkalosis was evaluated. Urine pH, serum bicarbonate, and urine Pco2-blood Pco2 studies were consistent with the diagnosis of distal renal tubular acidosis (RTA-type I). Analysis of serum potassium and chloride levels during periods of alkalosis and acidosis revealed that potassium depletion and hypochloremic volume contraction served to maintain the alkalotic state despite the presence of an underlying chronic acidosis. This case represents an unusual presentation for renal tubular acidosis and suggests that, under certain conditions, renal tubular acidosis may predispose to the maintenance of a metabolic alkalosis.

Effect of potassium depletion on chloride transport in the loop of Henle in the rat

1985 ◽  
Vol 248 (5) ◽  
pp. F682-F687 ◽  
Author(s):  
R. G. Luke ◽  
B. B. Booker ◽  
J. H. Galla
Keyword(s):  
Chloride Transport ◽  
Chloride Concentration ◽  
Distal Tubule ◽  
Normal Diet ◽  
Potassium Depletion ◽  
Thick Ascending Limb ◽  
Loop Of Henle ◽  
Chloride Absorption ◽  
Altered Response ◽  
And Control

Microperfusion of the superficial loop segment (latest proximal to earliest distal tubule) was performed in potassium-depleted and control rats. Potassium depletion was confirmed by analysis of muscle content (control 45 +/- 2, potassium depletion 33.5 +/- 0.9 meq/100 g dry solids). During perfusion at 20 nl/min net chloride absorption was decreased (66 +/- 3 vs. 77 +/- 2%, P less than 0.01) and early distal chloride concentration increased (70 +/- 5 vs. 50 +/- 4 meq/liter, P less than 0.01) in the potassium-depleted rats. In separate paired experiments in potassium-depleted rats, indomethacin infusion increased net chloride absorption (P less than 0.05) and lowered early distal chloride concentration (P less than 0.05) toward, but not to, normal. A similar effect of indomethacin to decrease early distal chloride concentration was seen in rats ingesting a normal diet and in control rats. We conclude that in potassium-depleted rats there is impaired net chloride absorption in the loop segment, most likely in the thick ascending limb, and that this effect is not produced by an altered response to prostaglandins. This defect in chloride transport may be responsible, at least in part, for the impaired concentrating capacity seen in potassium-depleted rats.

Effect of potassium depletion and protein intake in vivo on renal tubular bicarbonate transport in vitro

1987 ◽  
Vol 252 (3) ◽  
pp. F509-F516 ◽  
Author(s):  
T. D. McKinney ◽  
K. K. Davidson
Keyword(s):  
Potassium Depletion ◽  
Co2 Absorption ◽  
Urine Ph ◽  
Outer Medulla ◽  
Acid Urine ◽  
Arterial Blood ◽  
Blood Ph ◽  
Renal Tubular ◽  
Collecting Tubules

These studies evaluated the effect of decreased dietary potassium and increased dietary protein content in rabbits on systemic acid-base parameters, urine pH, and segmental renal tubular bicarbonate handling in vitro. Animals fed a potassium-deficient high-protein diet (KD) for 2 wk developed metabolic acidosis (arterial blood pH 7.31 vs. 7.43) and excreted a more acid urine than control animals fed a diet with normal amounts of potassium and protein; whereas, animals fed the same potassium deficient diet to which supplemental potassium was added (KD + K+) excreted an even more acid urine and had a blood pH of 7.36. In superficial proximal convoluted and straight tubules, there were no differences in rates of fluid and total CO2 absorption between control and KD tubules. Cortical collecting tubules obtained from KD and KD + K+ animals absorbed, and control tubules secreted total CO2 in vitro. With an ambient potassium concentration of 2.5 mM, collecting tubules obtained from the inner stripe of the outer medulla of KD animals absorbed significantly less total CO2 than control tubules. The same tendency was observed in collecting tubules from the outer stripe of the outer medulla. Plasma aldosterone levels fell with development of potassium depletion. Administration of deoxycorticosterone for 1 day to KD animals was associated with a lower urine pH and higher arterial blood pH than in untreated KD animals and with increased total CO2 absorption by both cortical collecting tubules and tubules from the inner stripe of the outer medulla.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of NaCl on renin and aldosterone responses to potassium depletion

1983 ◽  
Vol 244 (2) ◽  
pp. E164-E169 ◽  
Author(s):  
T. A. Kotchen ◽  
G. P. Guthrie ◽  
J. H. Galla ◽  
R. G. Luke ◽  
W. J. Welch
Keyword(s):  
Plasma Renin Activity ◽  
Volume Expansion ◽  
Chloride Transport ◽  
Plasma Renin ◽  
Plasma Aldosterone ◽  
Renin Secretion ◽  
Renin Activity ◽  
Potassium Depletion ◽  
Thick Ascending Limb ◽  
Loop Of Henle

We have previously suggested that renin secretion is inversely related to the magnitude of absorptive chloride transport in the thick ascending limb of the loop of Henle. Potassium depletion inhibits chloride transport at this site in the nephron. Consequently, we studied the effects of varying sodium and chloride intakes on the renin and aldosterone responses to potassium depletion. Potassium depletion prevented suppression of plasma renin activity (PRA) by dietary NaCl loading and augmented the PRA response to NaCl deprivation. PRA was stimulated (P less than 0.01) by selective chloride (without sodium) deprivation, and potassium depletion did not augment this response. Potassium depletion did not interfere with suppression of PRA by albumin-induced volume expansion. Plasma aldosterone was suppressed by potassium depletion, and the effect of potassium depletion on aldosterone was augmented by NaCl deprivation. In conclusion, the magnitude of PRA stimulation and aldosterone suppression by potassium depletion is modulated by dietary NaCl intake. The results are consistent with the hypothesis that potassium depletion stimulates renin release by inhibiting chloride transport in the loop of Henle.

Mechanism for inhibition of renin release by acute plasma volume expansion in the dog

1985 ◽  
Vol 248 (2) ◽  
pp. F206-F211 ◽  
Author(s):  
M. W. Roy ◽  
C. E. Ott ◽  
W. J. Welch ◽  
J. H. Downs ◽  
T. A. Kotchen
Keyword(s):  
Plasma Volume ◽  
Volume Expansion ◽  
Chloride Transport ◽  
Renin Secretion ◽  
Renin Release ◽  
Renal Nerves ◽  
Plasma Volume Expansion ◽  
Renal Nerve ◽  
Albumin Infusion ◽  
Renal Tubular

Plasma volume expansion alters renal tubular sodium chloride transport and renal nerve activity. The purpose of this study was to determine the mechanism(s) for inhibition of renin secretion by acute volume expansion with albumin in the anesthetized dog. In dogs with a single intact kidney, albumin infusion decreased renin release by 86% and significantly increased renal blood flow, glomerular filtration rate, and sodium excretion. Albumin volume expansion inhibited renin secretion to a lesser extent in dogs with denervated filtering kidneys and in dogs with innervated nonfiltering kidneys. In dogs with denervated nonfiltering kidneys, albumin infusion did not change renin secretion. Comparable volume expansion was produced in all groups. Thus, inhibition of renin release by acute plasma volume expansion is dependent on both a renal tubular mechanism and the integrity of the renal nerves. Partial inhibition of renin release was observed with interruption of either one of the mechanisms, whereas interruption of both mechanisms totally abolished the effect of acute plasma volume expansion on renin secretion.

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