An Economy of Water in Renal Function Referable to Urea

Gamble, James L.; McKhann, Charles F.; Butler, Allan M.; Tuthill, Elizabeth

doi:10.1152/ajplegacy.1934.109.1.139

Cited by 169 publications

(100 citation statements)

References 0 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The points are more widely scattered in the lower range of values for urine volume and osmolar content, probably because urine volume is more apt to be determined by its urea content at these lower rates of salt and glucose excretion. As has been shown in the rat (9) with salt and glucose. Our data suggest that the human kidney behaves toward salt, glucose, and urea in a manner similar to that of the rat.…”

Section: Plan Of Studysupporting

confidence: 66%

Chloride Excretion During Glycosuria in Patients With Diabetes

Gabrilove¹

1946

J. Clin. Invest.

View full text Add to dashboard Cite

Section: Plan Of Studysupporting

confidence: 66%

Chloride Excretion During Glycosuria in Patients With Diabetes

Gabrilove¹

1946

J. Clin. Invest.

View full text Add to dashboard Cite

“…Urea's importance has been appreciated for nearly 8 decades, since Gamble et al first described "an economy of water in renal function referable to urea" (19). Protein deprivation reduces maximal urine concentrating ability and is restored by urea infusion or correction of the protein malnutrition (11,16).…”

Section: Urine Concentrating Mechanismmentioning

confidence: 99%

Urea and Ammonia Metabolism and the Control of Renal Nitrogen Excretion

Weiner

Mitch

Sands

2015

Clinical Journal of the American Society of Nephrology

348

265

View full text Add to dashboard Cite

Renal nitrogen metabolism primarily involves urea and ammonia metabolism, and is essential to normal health. Urea is the largest circulating pool of nitrogen, excluding nitrogen in circulating proteins, and its production changes in parallel to the degradation of dietary and endogenous proteins. In addition to serving as a way to excrete nitrogen, urea transport, mediated through specific urea transport proteins, mediates a central role in the urine concentrating mechanism. Renal ammonia excretion, although often considered only in the context of acidbase homeostasis, accounts for approximately 10% of total renal nitrogen excretion under basal conditions, but can increase substantially in a variety of clinical conditions. Because renal ammonia metabolism requires intrarenal ammoniagenesis from glutamine, changes in factors regulating renal ammonia metabolism can have important effects on glutamine in addition to nitrogen balance. This review covers aspects of protein metabolism and the control of the two major molecules involved in renal nitrogen excretion: urea and ammonia. Both urea and ammonia transport can be altered by glucocorticoids and hypokalemia, two conditions that also affect protein metabolism. Clinical conditions associated with altered urine concentrating ability or water homeostasis can result in changes in urea excretion and urea transporters. Clinical conditions associated with altered ammonia excretion can have important effects on nitrogen balance.

show abstract

“…Urea's importance to the generation of a concentrated urine has been appreciated since at least 1934. 1,2 Several studies have shown that maximal urine concentrating ability is decreased in protein-deprived mammals and is restored by urea infusion. 3 More recently, a UT-A1/UT-A3 knock-out mouse, 4,5 a UT-A2 knock-out mouse, 6 and a UT-B knock-out mouse [7][8][9] were each shown to have urine concentrating defects.…”

mentioning

confidence: 99%

Epac Regulates UT-A1 to Increase Urea Transport in Inner Medullary Collecting Ducts

Wang

Klein

Blount

et al. 2009

Journal of the American Society of Nephrology

View full text Add to dashboard Cite

Urea plays a critical role in the concentration of urine, thereby regulating water balance. Vasopressin, acting through cAMP, stimulates urea transport across rat terminal inner medullary collecting ducts (IMCD) by increasing the phosphorylation and accumulation at the apical plasma membrane of UT-A1. In addition to acting through protein kinase A (PKA), cAMP also activates Epac (exchange protein activated by cAMP). In this study, we tested whether the regulation of urea transport and UT-A1 transporter activity involve Epac in rat IMCD. Functional analysis showed that an Epac activator significantly increased urea permeability in isolated, perfused rat terminal IMCD. Similarly, stimulating Epac by adding forskolin and an inhibitor of PKA significantly increased urea permeability. Incubation of rat IMCD suspensions with the Epac activator significantly increased UT-A1 phosphorylation and its accumulation in the plasma membrane. Furthermore, forskolin-stimulated cAMP significantly increased ERK 1/2 phosphorylation, which was not prevented by inhibiting PKA, indicating that Epac mediated this phosphorylation of ERK 1/2. Inhibition of MEK 1/2 phosphorylation decreased the forskolin-stimulated UT-A1 phosphorylation. Taken together, activation of Epac increases urea transport, accumulation of UT-A1 at the plasma membrane, and UT-A1 phosphorylation, the latter of which is mediated by the MEK-ERK pathway.

show abstract

An Economy of Water in Renal Function Referable to Urea

Cited by 169 publications

References 0 publications

Chloride Excretion During Glycosuria in Patients With Diabetes

Chloride Excretion During Glycosuria in Patients With Diabetes

Urea and Ammonia Metabolism and the Control of Renal Nitrogen Excretion

Epac Regulates UT-A1 to Increase Urea Transport in Inner Medullary Collecting Ducts

Contact Info

Product

Resources

About