Impairment of renal medullary osmolyte accumulation in potassium-depleted rats

1994 ◽  
Vol 267 (1) ◽  
pp. F139-F145 ◽  
Author(s):  
T. Nakanishi ◽  
Y. Takamitsu ◽  
H. Nakahama ◽  
M. Sugita
Keyword(s):  
Water Deprivation ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Untreated Group ◽  
Urinary Concentration ◽  
Potassium Depletion ◽  
Water Diuresis ◽  
Osmolyte Accumulation ◽  
Group Water ◽  
The Relationship

To determine the relationship between accumulation of osmolytes and maximal urinary concentration in potassium depletion, we tested the effects of experimental water diuresis or potassium depletion on osmolytes in the renal medulla of rats. Hyperosmotic stress was imposed by 4 days of water deprivation for the purpose of establishing the maximal concentrating ability or by the infusion of sodium for the purpose of loading the equal amounts of sodium to the renal medulla. In the diuresis group, water deprivation failed to increase betaine, sorbitol, and taurine contents to the same level as the untreated group, although sodium infusion increased betaine and sorbitol. In the potassium depletion group followed by water deprivation, urine osmolality (2,490 +/- 241 vs. 3,425 +/- 268 mosmol/kgH2O) and all osmolytes were significantly lower than in the untreated group. In response to hyperosmolality with sodium infusion, myo-inositol and glycerophosphorylcholine contents rose to the level of the untreated group. Medullary betaine (67.6 +/- 6.8 vs. 99.5 +/- 8.9), taurine (44.7 +/- 2.4 vs. 61.4 +/- 6.2) and sorbitol (35.6 +/- 4.4 vs. 57.0 +/- 8.4 mmol/kg protein) contents were reduced in potassium-depleted rats when the renal medulla was as hypertonic as in the untreated group. In conclusion, the processing of betaine, taurine, and sorbitol accumulation appeared to be impaired in potassium depletion.

Increased PGE2 excretion by dDAVP in humans depends on state of hydration

1986 ◽  
Vol 250 (6) ◽  
pp. F1008-F1012 ◽  
Author(s):  
U. Schwertschlag ◽  
J. G. Gerber ◽  
J. S. Barnes ◽  
A. S. Nies
Keyword(s):  
Water Deprivation ◽  
Urine Volume ◽  
Plasma Osmolality ◽  
Urine Osmolality ◽  
Water Diuresis ◽  
Water Load ◽  
Water Ingestion ◽  
Transient Rise ◽  
Relationship Of ◽  
The Relationship

The relationship of renal prostaglandin E2 (PGE2) excretion (UPGEV) to water deprivation, water diuresis, and subsequent antidiuresis by 1-desamino-8-D-arginine vasopressin (dDAVP) was studied in female volunteers. After 16 h of water deprivation, the subjects began a sustained water diuresis for 8 h. This diuresis caused a transient twofold rise in UPGEV at 2 h (P less than 0.05), which then fell back to or below baseline levels. dDAVP given during the water diuresis caused a transient rise of UPGEV as urine volume decreased and plasma osmolality fell from 277 +/- 1.5 to 271 +/- 2 mosmol/kg (P less than 0.01). Another group of subjects had the water diuresis discontinued after 4 h with dDAVP given at the 5th h when urine volume was decreasing and urine osmolality was increasing. In this setting dDAVP did not produce as great a fall in plasma osmolality nor did it increase UPGEV. These data indicate that renal prostaglandin synthesis (as determined by UPGEV) is increased transiently by an acute water load; dDAVP given during continued water ingestion results in a fall in plasma osmolality and increased PGE excretion; however, dDAVP does not increase UPGEV during normal hydration; and UPGEV is independent of changes in urine flow. These findings imply that renal prostaglandins may have a functional role in humans to inhibit the hydroosmotic actions of antidiuretic hormone, and thus hasten the excretion of a water load, and to prevent overhydration when inappropriate antidiuresis occurs. However, there is no evidence that the stimulus for prostaglandin production is dDAVP per se.

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.

scholarly journals Race, sex, and the regulation of urine osmolality: observations made during water deprivation

2010 ◽  
Vol 299 (3) ◽  
pp. R977-R980 ◽  
Author(s):  
Michael L. Hancock ◽  
Daniel G. Bichet ◽  
George J. Eckert ◽  
Lise Bankir ◽  
Mary Anne Wagner ◽  
...  
Keyword(s):  
Water Conservation ◽  
Water Deprivation ◽  
Collecting Duct ◽  
Urine Osmolality ◽  
Thick Ascending Limb ◽  
Race Difference ◽  
Water Reabsorption ◽  
Blacks And Whites ◽  
Relationship Of ◽  
The Relationship

A more concentrated urine is excreted by blacks than whites and by men than women. The purpose of this study was to explore the physiological bases for the race and sex effects during water deprivation when osmoregulation is challenged and differences are amplified. Drinking water was withheld from 17 blacks (10 men) and 19 whites (9 men) for 24 h. Vasopressin (VP) levels and osmolality in plasma (Posmol) and urine (Uosmol) were measured basally and then every 4 h. Uosmol was higher in blacks at baseline ( P = 0.01) and during water deprivation ( P = 0.046). Before and during water deprivation, no differences were seen in levels of VP, Posmol, or the VP-Uosmol relationship between blacks and whites. Although VP levels were initially higher in men ( P < 0.02 for samples collected over the first 12 h), over the last 12 h of water deprivation, Uosmol was higher ( P = 0.027) and more responsive to the level of VP (in terms of slopes, P = 0.0001) in women than men. Our results suggest that, after a period of water deprivation, there develops a sensitivity of the collecting duct to VP that is greater in women. Although Uosmol is higher in blacks, the race difference in water conservation did not appear to result from differences in the level of VP or the sensitivity of the collecting duct to VP. Upstream effects such as Na+ uptake in the thick ascending limb, with its ensuing effects on water reabsorption, need to be considered in future studies of the relationship of race to water conservation.

scholarly journals mPGES-1 deletion potentiates urine concentrating capability after water deprivation

2012 ◽  
Vol 302 (8) ◽  
pp. F1005-F1012 ◽  
Author(s):  
Zhanjun Jia ◽  
Gang Liu ◽  
Maicy Downton ◽  
Zheng Dong ◽  
Aihua Zhang ◽  
...  
Keyword(s):  
Water Deprivation ◽  
Potential Role ◽  
Urine Volume ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Protein Abundance ◽  
Wild Type ◽  
Control Groups ◽  
Urine Concentrating Ability

PGE2 plays an important role in the regulation of fluid metabolism chiefly via antagonizing vasopressin-induced osmotic permeability in the distal nephron, but its enzymatic sources remain uncertain. The present study was undertaken to investigate the potential role of microsomal PGE synthase (mPGES)-1 in the regulation of urine concentrating ability after water deprivation (WD). Following 24-h WD, wild-type (WT) mice exhibited a significant reduction in urine volume, accompanied by a significant elevation in urine osmolality compared with control groups. In contrast, in response to WD, mPGES-1 knockout (KO) mice had much less urine volume and higher urine osmolality. Analysis of plasma volume by measurement of hematocrit and by using a nanoparticle-based method consistently demonstrated that dehydrated WT mice were volume depleted, which was significantly improved in the KO mice. WD induced a twofold increase in urinary PGE2 output in WT mice, which was completely blocked by mPGES-1 deletion. At baseline, the KO mice had a 20% increase in V2 receptor mRNA expression in the renal medulla but not the cortex compared with WT controls; the expression was unaffected by WD irrespective of the genotype. In response to WD, renal medullary aquaporin-2 (AQP2) mRNA exhibited a 60% increase in WT mice, and this increase was greater in the KO mice. Immunoblotting demonstrated increased renal medullary AQP2 protein abundance in both genotypes following WD, with a greater increase in the KO mice. Similar results were obtained by using immunohistochemistry. Paradoxically, plasma AVP response to WD seen in WT mice was absent in the KO mice. Taken together, these results suggest that mPGES-1-derived PGE2 reduces urine concentrating ability through suppression of renal medullary expression of V2 receptors and AQP2 but may enhance it by mediating the central AVP response.

Characterization of organic osmolytes in avian renal medulla: a nonurea osmotic gradient system

1993 ◽  
Vol 264 (6) ◽  
pp. R1045-R1049
Author(s):  
Y. H. Lien ◽  
M. M. Pacelli ◽  
E. J. Braun
Keyword(s):  
Water Deprivation ◽  
Renal Cortex ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Gradient System ◽  
Osmotic Gradient ◽  
Organic Osmolytes ◽  
Before And After ◽  
Avian Kidney

We measured the organic osmolytes present in the renal cortex and medullary cones of adult female domestic fowl before and after 48 h of water deprivation. Urine osmolality increased from 198 +/- 82 to 569 +/- 42 mosmol/kgH2O after water deprivation. In water-deprived birds, the major organic osmolytes, myoinositol, betaine, and taurine, in the medullary cones increased by 40, 100, and 24%, respectively, compared with control birds. No sorbitol was detected, and glycerophosphorylcholine (GPC) content was not affected by water deprivation. In the renal cortex, only betaine content increased significantly (4.8 +/- 0.6 vs. 3.1 +/- 0.3 mmol/kg wet wt) after water deprivation. In this study, we demonstrated that birds, like mammals, accumulate organic osmolytes in response to the increased interstitial osmolality that occurs during antidiuresis. Because urea is nearly absent in the avian medullary interstitium, our observation that GPC is not osmoregulated in the avian kidney supports the idea that GPC is the “counteracting osmolyte” for urea in the mammalian kidney. Furthermore, the organic osmolytes present in avian medullary cones are remarkably similar to those of the mammalian outer medulla. This similarity may be relevant to the morphological analogy of the two regions.

Normal Urine Concentrating Ability in Magnesium Depletion

1972 ◽  
Vol 43 (6) ◽  
pp. 723-729 ◽  
Author(s):  
S. M. Suh ◽  
J. Sellors
Keyword(s):  
Water Deprivation ◽  
Urine Osmolality ◽  
Urine Concentration ◽  
Potassium Depletion ◽  
Magnesium Depletion ◽  
Normal Urine ◽  
Urine Concentrating Ability

1. We studied urine concentrating ability in ten magnesium-depleted puppies and compared the results with those of match-fed, littermate controls. 2. The experimental puppies became hypomagnesaemic and hypocalcaemic without evidence of potassium depletion. After 24 h of food and water deprivation, urine osmolality increased to 1350 ± 340 mosm/kg of water. This value did not differ from that of control animals. 3. We also studied urine concentrating ability in a child with primary hypomagnesaemia and secondary hypocalcaemia. He could achieve a urine concentration of 1080 mosm/kg of water after 20 h of water deprivation when he was hypomagnesaemic and hypocalcaemic. 4. We conclude that urine concentrating ability is normal in magnesium depletion uncomplicated by hypercalcaemia or severe potassium depletion.

The Role of Vasopressin and Urea in the Renal Concentrating Defect of Patients with Cirrhosis of the Liver

1971 ◽  
Vol 41 (5) ◽  
pp. 441-452 ◽  
Author(s):  
C. A. Vaamonde ◽  
Liliana S. Vaamonde ◽  
J. I. Presser ◽  
H. J. Morosi ◽  
E. L. Klingler ◽  
...  
Keyword(s):  
Urine Osmolality ◽  
Urine Flow ◽  
Cirrhosis Of The Liver ◽  
Urinary Concentration ◽  
Renal Tubules ◽  
Urea Synthesis ◽  
Water Diuresis ◽  
Flow Rates ◽  
Cirrhotic Patients ◽  
Concentrating Defect

1. The maximal urine osmolality in response to vasopressin during water diuresis and during hydropenia was studied in twenty patients with cirrhosis and sixteen noncirrhotic subjects under controlled dietary conditions. 2. The cirrhotic patients exhibited a significantly lower maximal urine osmolality under both experimental conditions. 3. During water diuresis decompensated and compensated cirrhotics had comparable maximal urine osmolalities after vasopressin. A decreased response of the renal tubules to vasopressin does not appear to have a significant role in the concentrating defect. 4. The cirrhotic patients had a significantly lower excretion rate of urea at high (water diuresis) and low (vasopressin antidiuresis or hydropenia) urine flow rates. The lower urine urea concentration accounted for most of the decrease observed in maximal urinary concentration. After vasopressin administration the absolute tubular reabsorption of urea was also significantly lower in cirrhotic patients. The results suggest that a decrease in the medullary urea content decreases medullary osmolality resulting in the defect in urine concentration noted in these cirrhotic patients at low urine flow rates. 5. Protein depletion or decreased urea synthesis may in part be responsible for the decreased availability of urea for the concentrating process in cirrhosis. 6. Lack of correlation between concentrating and diluting capacity in these patients suggested that decreased delivery of sodium to the distal site might not be the limiting factor common to both renal functional abnormalities observed in cirrhosis of the liver.

scholarly journals Role of countercurrent multiplication in renal ammonium handling: regulation of medullary ammonium accumulation.

1991 ◽  
Vol 2 (1) ◽  
pp. 77-83 ◽  
Author(s):  
R K Packer ◽  
S S Desai ◽  
K Hornbuckle ◽  
M A Knepper
Keyword(s):  
Water Deprivation ◽  
Renal Medulla ◽  
Ammonium Concentration ◽  
Ammonium Excretion ◽  
Acid Base ◽  
Water Diuresis ◽  
Outer Medulla ◽  
Ammonia Content ◽  
Ammonium Accumulation ◽  
Total Ammonia

Ammonium (NH3 plus NH4+), produced predominantly in the proximal tubule, is transferred to the final urine by a process involving countercurrent multiplication of ammonium which generates an ammonium concentration gradient in the renal medulla. It was hypothesized that if urinary ammonium excretion rates are controlled in part by the medullary ammonium gradient, changes in hydration and acid-base state should cause changes in the medullary ammonium gradient consistent with expected changes in urinary ammonium concentrations. To test that hypothesis, rats were subjected to water diuresis, water deprivation, water deprivation plus furosemide, and dietary acid and base loads and corticomedullary ammonium gradients in their kidneys were then measured. Sections were cut along the corticomedullary axis to yield slices of cortex, outer stripe of outer medulla, inner stripe of outer medulla, and three levels of the inner medulla. The total ammonia content of homogenized slices was measured by either a membrane ammonia electrode or an enzymatic technique. Kidneys from water-deprived animals showed a distinct ammonium gradient along the corticomedullary axis, with the highest contents found at the tip of the papilla. The gradient was attenuated by water diuresis and abolished by furosemide. Acid loading enhanced the gradient, and base loading abolished it. These results indicate that the corticomedullary ammonium gradient is regulated in response to changes in hydration and acid-base state.

Effects of fluid intake on basal and vasopressin-responsive urinary prostaglandin E

1983 ◽  
Vol 245 (1) ◽  
pp. F48-F57
Author(s):  
H. T. Campbell ◽  
P. A. Craven ◽  
F. R. DeRubertis
Keyword(s):  
Water Intake ◽  
Water Deprivation ◽  
Fluid Intake ◽  
Urine Volume ◽  
Urine Osmolality ◽  
Prostaglandin E ◽  
Water Diuresis ◽  
Water Load ◽  
Ad Libitum ◽  
Ad Libitum Intake

The effects of fluid intake on basal and vasopressin-responsive urinary PGE excretion (UPGEV) were examined in conscious rats under conditions of 1) ad libitum water intake, 2) water deprivation, and 3) water diuresis induced by ad libitum intake of 5% dextrose in water. UPGEV fell progressively during 40 h of water deprivation. Water diuresis after water deprivation increased UPGEV transiently (8 h). Vasopressin (Pitressin tannate in oil, 5 U/kg subcutaneously) increased UPGEV and decreased urine volume (V) in rats on ad libitum water intake but did not alter UPGEV during water deprivation. Indomethacin suppressed UPGEV (70-90%), increased basal urine osmolality (Uosmol), and potentiated the antidiuretic response to Pitressin in rats on ad libitum water intake. Indomethacin accelerated by 8 h the onset of maximal antidiuresis in water-deprived rats but did not significantly alter water balance. During water diuresis, UPGEV declined in the first 8 h after Pitressin. Thereafter, UPGEV increased markedly, concurrent with early vasopressin escape. Indomethacin or meclofenamate inhibited the rise in UPGEV, the decline in Uosmol, and the increase in V of the escape phase. Indomethacin or meclofenamate also impaired the excretion of an acute water load (5% body wt) given during escape. The spontaneous decline in UPGEV during hydropenia may serve to maximize physiologic antidiuresis. Conversely, the marked increase in UPGEV induced by administration of vasopressin during water diuresis may serve to suppress the antidiuretic response and thus play a role in the mediation of escape from physiologically inappropriate antidiuresis.

Water removal and solute additions determining increases in renal medullary osmolality

1983 ◽  
Vol 244 (5) ◽  
pp. F472-F482 ◽  
Author(s):  
B. Schmidt-Nielsen ◽  
B. Graves ◽  
J. Roth
Keyword(s):  
Water Content ◽  
Wistar Rats ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Water Removal ◽  
Water Diuresis ◽  
Outer Medulla ◽  
Tissue Removal ◽  
Males And Females

Osmolality and solute concentrations of the mammalian renal medulla increase and decrease with changing urine osmolality. These changes are brought about by addition or removal of solute or water to or from the renal medullary tissue. In Munich-Wistar rats and Syrian hamsters, males and females, actual amounts of and the various solutes involved in these changes were determined. Kidneys were removed from animals killed in different stages of water diuresis and antidiuresis. The renal medulla was analyzed by a new method that permits determination of water and solutes on the same piece of tissue. Removal of water and addition of urea were the two most important factors in raising inner medullary osmolality. Papillary water content was inversely related to the papillary osmolality and was 50% lower in extreme antidiuresis compared with water diuresis. Rats had higher papillary water content than hamsters. In the outer medulla, water removal was significant in the hamsters but not in the rats. Addition of urea to the papillary tissue exceeded the osmotic equivalent of NaCl by a factor of 2.8 in both rats and hamsters. Females of both species showed greater changes than males in amounts of urea in the inner medulla.

Sign in / Sign up

Export Citation Format

Share Document