Potassium and sodium excretion and potassium homeostasis during acute hypokalemia

1965 ◽  
Vol 208 (6) ◽  
pp. 1143-1152 ◽  
Author(s):  
Robert R. Siegel ◽  
William D. Lotspeich
Keyword(s):  
Sodium Excretion ◽  
Extracellular Fluid ◽  
Tubular Secretion ◽  
Urine Flow ◽  
Potassium Excretion ◽  
Distal Nephron ◽  
Close Coupling ◽  
Potassium Homeostasis ◽  
Blood Ph ◽  
Total Body

Decreased potassium and increased sodium excretion were observed in dogs acutely potassium-depleted by hemodialysis. Potassium excretion at constant blood pH varied directly with plasma [K+]. When filtered Na load and urine flow were constant during K+ depletion, increase in Na excretion was equivalent to decrease in K+ excretion, suggesting close coupling between transtubular movements of the two ions. Large changes in plasma [K+] (30%) and K+ excretion (50%) were produced with removal of a relatively small amount (estimated 3%) of total body K+. Plasma [K+] decrease during depletion was rapidly decelerated by movement of intracellular K+ into the extracellular fluid (ECF). When ECF [K+] stabilized, further decrease in K+ excretion ceased despite continued reduction of total body K+. It appears: 1) that tubular secretion of K+ is directly and rapidly responsive to reduction in ECF [K+]; 2) that low ECF [K+] may simultaneously impair contraluminal K+ uptake and Na extrusion, reducing K+ excretion and Na reabsorption during acute hypokalemia. Stoichiometry of changes suggests a 1:1 coupling between K+ secretion and moiety of Na reabsorption in the distal nephron.

Role of vasopressin in maintenance of potassium homeostasis in severe hemorrhage

2013 ◽  
Vol 305 (2) ◽  
pp. R101-R103 ◽  
Author(s):  
Catherine F. T. Uyehara ◽  
Joy Sarkar
Keyword(s):  
Sharp Increase ◽  
Plasma Potassium ◽  
Urine Flow ◽  
Potassium Excretion ◽  
Volume Loss ◽  
Distal Nephron ◽  
Potassium Homeostasis ◽  
Normal Limits ◽  
Severe Hemorrhage

Uncontrolled elevation in plasma potassium within minutes of rapid blood volume loss is associated with mortality and distinguishes nonsurvivors of severe hemorrhage from survivors. In a pig model of severe hemorrhage, we discovered that along with a sharp increase in plasma potassium coincident with a shut down of urine flow, nonsurvivors also had an insufficient vasopressin response to hemorrhage. In contrast, survivors did have elevated vasopressin levels in response to hemorrhage and maintained plasma potassium within normal limits. While it has been demonstrated for some time that vasopressin can influence secretion of potassium in the distal nephron, the magnitude of this effect and conditions under which this contributes to physiological modulation of potassium excretion has yet to be defined. In this review, we assess the evidence that would suggest that vasopressin plays a key role in modulating potassium excretion and is important in the regulation of potassium homeostasis during hemorrhage.

Homeostatic potassium excretion in fed and fasted sheep

1988 ◽  
Vol 254 (2) ◽  
pp. R357-R380 ◽  
Author(s):  
L. Rabinowitz ◽  
D. M. Green ◽  
R. L. Sarason ◽  
H. Yamauchi
Keyword(s):  
Flow Rate ◽  
Urine Flow ◽  
Plasma Aldosterone ◽  
Urine Flow Rate ◽  
Potassium Excretion ◽  
Adult Sheep ◽  
Blood Ph ◽  
Low Levels ◽  
K Concentration ◽  
Filtered Load

In unanesthetized adult sheep, following intake of a daily meal, there was a peak in K excretion. The maximum and minimum rates of K excretion following meals were directly related to meal K content. On days without meals, no peak in K excretion occurred. Changes in K excretion on fed and fast days occurred without changes in the low levels of plasma aldosterone and were poorly correlated with urine or blood pH, urine flow rate, Na excretion, or the filtered load of K, but they correlated well with fractional K excretion. Plasma K did not change on fast days. Plasma K increased on some, but not all, fed days. Increases in plasma K that occurred on fed days were insufficient to account for the concurrent kaliuresis. Infusion of aldosterone or isotonic NaCl failed to alter K excretion in fed or fasted sheep. Infusion of isotonic NaCl + aldosterone hypertonic Na2SO4 + aldosterone increased K excretion in fasted but not fed sheep. Infusion of K in the rumen of fed and fasted sheep elevated rumen K concentration and led to increases in K excretion that could not be explained by increases in plasma K. The mechanisms responsible for the homeostatic changes in K excretion on fed and fast days were not ascertained but may importantly depend on sensors of enteric K content.

Interstitial dynamics in rats with early stage experimental cirrhosis of the liver

1989 ◽  
Vol 256 (3) ◽  
pp. F497-F503
Author(s):  
E. Sanz ◽  
C. Caramelo ◽  
J. M. Lopez-Novoa
Keyword(s):  
Sodium Excretion ◽  
Interstitial Fluid ◽  
Early Stage ◽  
Fluid Pressure ◽  
Extracellular Fluid ◽  
Ringer Solution ◽  
Urine Flow ◽  
Cirrhosis Of The Liver ◽  
Experimental Cirrhosis ◽  
Albumin Infusion

Pathogenesis of edema in cirrhosis of the liver is still incompletely understood. The present study was designed to examine interstitial fluid dynamics in cirrhotic, non-ascitic rats, measuring interstitial fluid pressure by means of a subcutaneous plastic capsule in basal conditions during extracellular fluid volume expansion with Ringer solution and during albumin infusion. Urine flow and sodium excretion and plasma and interstitial fluid volumes were simultaneously measured. Cirrhotic rats exhibited reduced urine flow and sodium excretion, both in basal conditions and in response to expansion maneuvers. Plasma and interstitial fluid volumes were higher in cirrhotic than in control animals. Remarkable alterations were present in capsular pressures in cirrhotic rats. In the control rats, basal capsular pressure values were negative, and they increased after Ringer infusion and markedly decreased with albumin infusion. In contrast, in cirrhotic rats, basal capsular pressures were in the positive range and they remained nearly constant during ringer infusion and albumin administration. These results suggest that in cirrhotic rats there are significant alterations in systemic interstitial dynamics, even before ascites formation. Altered systemic capillary dynamics may therefore be important early changes that precede and thus contribute to the formation of edema in cirrhosis.

A vasopressin-mediated diminution of potassium excretion in water-loaded man

1985 ◽  
Vol 69 (5) ◽  
pp. 601-606 ◽  
Author(s):  
J. Buckley ◽  
E. M. Gebruers ◽  
W. J. Hall ◽  
N. M. B. Harrington
Keyword(s):  
Urine Osmolality ◽  
Urine Flow ◽  
Potassium Excretion ◽  
Distal Nephron ◽  
Water Diuresis ◽  
Specific Effects ◽  
Antidiuretic Effect ◽  
Endogenous Prostaglandins ◽  
Potassium Absorption ◽  
Prior Administration

1. Intravenous vasopressin (1–3 μ-units min−1 kg−1) had an antidiuretic effect on water-loaded man and also diminished potassium excretion. As noted by others, aspirin (2.4 g) enhanced the antidiuretic effect of vasopressin, but the fall in potassium excretion was not modified by prior administration of aspirin, which makes it unlikely that the fall was due to the release of endogenous prostaglandins. 2. After terminating the infusion of vasopressin, the fall in potassium output persisted longer than the antidiuresis, which makes it unlikely that the antikaliuretic effect of vasopressin is secondary to its effect on urine flow. 3. The unchanged antikaliuretic effect of vasopressin after aspirin treatment, together with its persistence after terminating the infusion, suggest the possible existence of vasopressin-mediated potassium absorption in the distal nephron in certain circumstances. 4. Aspirin administration had specific effects of its own in water-loaded man. It decreased both the water diuresis and sodium excretion but did not alter potassium excretion or urine osmolality.

Effect of vasopressin on sodium excretion and plasma antinatriferic activity in the dog

1976 ◽  
Vol 231 (1) ◽  
pp. 28-33 ◽  
Author(s):  
VM Buckalew ◽  
KA Dimond
Keyword(s):  
Glomerular Filtration Rate ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Urine Flow ◽  
Potassium Excretion ◽  
State Control ◽  
Sham Control ◽  
Anesthetized Dogs ◽  
Renal Tubular ◽  
Steady State Control

Vasopressin (VP) was administered for 1 h intravenously to hydropenic, anesthetized dogs in doses of 1.0-1.25 mU/kg per min. In 14 experiments, sodium excretion (UNA V) increased from a mean of 13 +/- 5 to a peak of 96 +/- 21 mueq/min 40 min after beginning infusion (P less than .001). Urine flow and potassium excretion increased from 0.18 +/-.04 ml/min and 20 +/- 2 meuq/min to peak values of 0.6 +/- .08 ml/min and 61 +/- 9 mueq/min, respectively (P less than .001), with no significant increase in glomerular filtration rate. No significant changes in UNA V occurred in eight sham control experiments of in six experiments in which VP was given at 75 muU/kf per min. To test the hypothesis that VP might be natriuretic indirectly by releasing a natriuretic substance, plasms ultrafiltrates were tested for toad bladder antinatriferic activity(AA). During steady-state control, AA was -10 +/- 3%. Thirty and sixty minutes after beginning VP, AA increased to -24 +/- 3% (P less than .05) and -26 +/- 2% (P less than .001), respectiviely. No significant change in plasma AA occurred in either sham controls or in animals given the subnatriuretic VP dose. Incubation of plasma with 1,000 muU/ml VP caused no increase in AA. The data show that VP natriuresis is accompanied by an increase in plasms AA. The results suggest that vasopressin natriuresis in hydropenic dogs at least in part to the release of a humoral inhibitor of renal tubular sodium transport.

Angiotensin and electrolyte excretion in renovascular hypertension

1965 ◽  
Vol 208 (6) ◽  
pp. 1087-1092 ◽  
Author(s):  
Abraham J. Borkowski ◽  
Stuart S. Howards ◽  
John H. Laragh
Keyword(s):  
Water Retention ◽  
Tubular Secretion ◽  
Urine Flow ◽  
Left Renal Artery ◽  
Potassium Excretion ◽  
Sodium Retention ◽  
Hypertensive Rats ◽  
Electrolyte Excretion ◽  
Water Excretion ◽  
Ureteral Catheterization

Under conditions of saline, urea, ADH infusion diuresis during anesthesia we observed that in normal rats angiotensin infusion regularly produced natriuresis and diuresis, the degree of which was more closely related to dosage than to increment in blood pressure. Potassium excretion often did not rise appreciably or actually fell during natriuresis, suggesting inhibition of tubular secretion. In animals with a clamp on the left renal artery in which hypertension did not ensue, the renal response to angiotensin was strikingly changed when studied by bilateral ureteral catheterization. Instead of diuresis the peptide produced either no effect or sodium and water retention in both kidneys. In the hypertensive rats, angiotensin consistently produced marked diuresis on the clipped side. Sodium excretion increased much more than urine flow. Simultaneously, in the opposite, unprotected kidney, angiotensin produced quite different effects—sodium and water excretion either did not change or were reduced. Renovascular reflexes and renal renin activity may be involved in determining whether angiotensin induces sodium retention or natriuresis.

Effect of Magnesium Deficiency and Excess on Renal Tubular Potassium Transport in the Rat

1981 ◽  
Vol 60 (5) ◽  
pp. 549-554 ◽  
Author(s):  
S. L. Carney ◽  
N. L. M. Wong ◽  
J. H. Dirks
Keyword(s):  
Magnesium Deficiency ◽  
Distal Tubule ◽  
Fractional Excretion ◽  
The Body ◽  
Control Group ◽  
Potassium Excretion ◽  
Potassium Homeostasis ◽  
Dietary Magnesium ◽  
Magnesium Status ◽  
Total Body

1. Dietary magnesium deficiency is commonly associated with significant potassium depletion although the mechanisms responsible are unknown. Because the kidney has an important role in both magnesium and potassium homeostasis, clearance and micropuncture experiments were performed on thyroparathyroidectomized magnesium-deficient, normal and hypermagnesaemic rats to study the effect of body magnesium status on renal potassium handling. 2. Dietary magnesium restriction that reduced total-body magnesium by 30% did not alter renal potassium excretion despite a 10% reduction in total-body potassium. Graded magnesium infusions increased the fractional excretion of potassium in both magnesium-depleted and normal rats. However, the increase in the dietary depleted group was significantly less than in the control group (5-10 and then 13% compared with 7-19 and then 28% respectively). These changes in urine potassium excretion followed alterations in distal-tubule function. Parathyroid hormone did not alter potassium excretion in any of the experimental groups in contrast with its effect on magnesium excretion. 3. These data support the concept of distal tubular control of renal potassium homeostasis. The body magnesium status appears to exert some control over cellular potassium content and to alter indirectly distal-tubule potassium excretion.

Atrial peptide potentiates renal responses to volume expansion in conscious dogs

1989 ◽  
Vol 256 (1) ◽  
pp. R284-R289
Author(s):  
C. H. Metzler ◽  
D. J. Ramsay
Keyword(s):  
Sodium Excretion ◽  
Urine Volume ◽  
Extracellular Fluid ◽  
Urinary Sodium Excretion ◽  
Urine Flow ◽  
Conscious Dogs ◽  
Physiological Dose ◽  
Peptide Secretion ◽  
Renal Responses ◽  
Dose Dependent

Experiments were performed to compare the renal responses to atrial peptide infusion in conscious dogs with normal and expanded extracellular fluid volumes to test the hypothesis that the renal responses to atrial peptide infusions are dependent on the prevailing fluid and electrolyte status in the animal. Atrial peptide-(99-126) was infused intravenously in doses of either 0, 5, 25, or 100 ng.kg-1.min-1 in conscious dogs prepared with chronic catheters in the femoral artery and vein and the urinary bladder. In dogs with normal extracellular fluid volume, atrial peptide caused small increases in urinary sodium excretion with the high physiological (25 ng.kg-1.min-1) and pharmacological (100 ng.kg-1.min-1) doses. Urine volume and potassium excretion were increased only at the highest pharmacological dose. In contrast, atrial peptide infusion in dogs that were volume expanded by infusion of hypertonic saline showed dramatic, dose-dependent increases in sodium excretion and urine flow with all doses tested. The low, physiological dose of atrial peptide (5 ng.kg-1.min-1) increased sodium excretion and urine flow rate in volume-expanded dogs more than the pharmacological dose in normal dogs (n = 4). These results demonstrate that the renal responses to atrial peptide infusion are potentiated in dogs that are volume expanded and suggest that under conditions where atrial peptide secretion would be enhanced, small changes in plasma atrial peptide concentration can have significant effects on renal function.

Natriuresis induced by localized perfusion within the third cerebral ventricle of sheep

1987 ◽  
Vol 252 (1) ◽  
pp. R1-R6 ◽  
Author(s):  
P. S. Cox ◽  
D. A. Denton ◽  
D. R. Mouw ◽  
E. Tarjan
Keyword(s):  
Sodium Excretion ◽  
Third Ventricle ◽  
Free Water ◽  
Sodium Concentration ◽  
Urine Flow ◽  
Cerebral Ventricle ◽  
Potassium Excretion ◽  
The Third ◽  
Anterior Dorsal ◽  
Sodium And Potassium

Push-pull perfusion was performed at four different sites in the third cerebral ventricle of conscious sheep. The recovery of the infused solution was 75–90%, suggesting a localized change in the ionic composition and osmolality restricted to a relatively small area in the cerebrospinal fluid (CSF). Sodium and potassium excretion and urine flow were studied before, during, and after perfusion of 200, 150, and 100 mM Na-CSF. Localized perfusion in the anterior dorsal third ventricle (AD3V) of 200 mM Na-CSF caused an increase in sodium and potassium excretion, in urine flow, and a decrease in free water clearance. Perfusion of 200 mM Na-CSF at the other three perfusion sites, i.e., anterior ventral third ventricle, posterior dorsal third ventricle, and posterior ventral third ventricle, did not influence sodium excretion and urine flow. Perfusions with 150 and 100 mM Na-CSF did not cause any change in sodium, potassium excretion, or urine flow at any of the four perfusion sites. These results suggest that sensors sensitive to changes of sodium concentration are located close to the ventricular surface in the anterior dorsal part of the third cerebral ventricle. When stimulated with increased sodium concentration they will initiate increased sodium excretion.

Effect of Vasopressin on Uric Acid Excretion: Evidence for Distal Nephron Reabsorption of Urate in Man

1976 ◽  
Vol 51 (1) ◽  
pp. 33-40 ◽  
Author(s):  
A. Meisel ◽  
H. Diamond
Keyword(s):  
Flow Rate ◽  
Distal Part ◽  
Extracellular Fluid ◽  
Urine Flow ◽  
Fluid Volume ◽  
Extracellular Fluid Volume ◽  
Urine Flow Rate ◽  
Distal Nephron ◽  
Uric Acid Excretion ◽  
Urate Reabsorption

1. When changes in urine flow rate were induced by vasopressin administration in eight subjects, urate excretion decreased by a mean of 14% and was positively correlated with urine flow rate (r = 0·88, p < 0·01). The effect of vasopressin on urate excretion was not influenced by prior changes in extracellular fluid volume. 2. Mannitol administration in a dose sufficient to prevent vasopressin-induced alterations in urine flow rate blocked the effect of vasopressin on urate excretion. 3. Alterations in urate excretion produced by changes in extracellular fluid volume could be distinguished from the urate-retaining effect of vasopressin-mediated decrease in urine flow. Urate retention after vasopressin was entirely attributed to a decrease in pyrazinamide-suppressible urate excretion, consistent with either decreased secretion or enhanced post-secretory reabsorption of urate. 4. Since diminished urine flow rate in the distal part of the nephron is more likely to lead to enhanced reabsorption of urate, these results provide additional evidence for urate reabsorption in the distal part of the nephron.

Sign in / Sign up

Export Citation Format

Share Document