The Effects of the Natriuretic Factor from Uremic Urine on Sodium Transport, Water and Electrolyte Content, and Pyruvate Oxidation by the Isolated Toad Bladder

Kaplan, Michael A.; Bourgoignie, Jacques J.; Rosecan, Jeffrey; Bricker, Neal S.

doi:10.1172/jci107707

Cited by 31 publications

(16 citation statements)

References 12 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The demonstration of an inhibitor of sodium transport with natriuretic activity in the plasma and urine of chronically uremic patients and animals has led to the suggestion that this substance is part of the effector limb of the physiologic control system regulating sodium excretion (3)(4)(5)(6)(7). Several lines of evidence (5,7) suggest that the presence of this natriuretic factor in concentrations detectable with the bioassay systems employed correlates with the dictates for and/or concurrent patterns of sodium excretion.…”

Section: Discussionmentioning

confidence: 99%

An inhibitor of sodium transport in the urine of dogs with normal renal function.

Favre¹,

Hwang²,

Schmidt³

et al. 1975

J. Clin. Invest.

View full text Add to dashboard Cite

AB STRA CT The urine and serum of chronically uremic patients and dogs contain an inhibitor of sodium transport that reduces short-circuit current (SCC) in the toad bladder and produces natriuresis in the rat. The present studies represent an effort to determine whether the same inhibitor is detectable in urine of normal dogs maintained on a sodium intake varying from 3 to 258 meq/day. Observations were made with and without fludrocortisone. The same Sephadex G-25 gel filtration fraction previously shown to contain the "uremic" inhibitor was tested in both the isolated toad bladder and rat bioassay systems. The fraction from dogs maintained on 258 meq sodium plus 0.2 mg fludrocortisone/day consistently inhibited SCC in the toad bladder and induced a natriuresis in the rat (P < 0.001). The fraction from dogs on the same sodium intake without fludrocortisone was also natriuretic (P <0.01) but did not inhibit SCC significantly. In contrast, the fraction from dogs fed 3 meq sodium with fludrocortisone or 91 meq sodium without fludrocortisone had no significant effect in either assay system. Thus, an inhibitor of sodium transport has been found in the urine of nonuremic dogs. Both the degree of natriuresis in the rat and the degree of inhibition of SCC in the toad bladder correlated with the state of sodium balance which ensued in the dog.

show abstract

Section: Discussionmentioning

confidence: 99%

An inhibitor of sodium transport in the urine of dogs with normal renal function.

Favre¹,

Hwang²,

Schmidt³

et al. 1975

J. Clin. Invest.

View full text Add to dashboard Cite

show abstract

“…Additional evidence supporting the existence of a natriuretic hormone includes experiments in which small-moleculecontaining fractions from serum (13) or urine extracts of CRD patients were shown to inhibit short-circuit current (SCC) across the frog skin (13,14) and toad bladder (15). These urine extracts also inhibited sodium transport in isolated perfused rabbit renal tubular collecting ducts (16).…”

mentioning

confidence: 99%

Identification of xanthurenic acid 8- O -β- d -glucoside and xanthurenic acid 8- O -sulfate as human natriuretic hormones

Cain¹,

Schroeder

Shankel³

et al. 2007

Proc. Natl. Acad. Sci. U.S.A.

Self Cite

View full text Add to dashboard Cite

showed that when these two variables were controlled, the kidney was still able to increase sodium excretion in response to a salt load. Several lines of evidence argued for a small-molecule signal as a definitive modulator of sodium excretion by the kidney. However, the chemical nature of the suspected natriuretic agent remained unknown. Here we report the identification and natriuretic activity of two closely related small molecules isolated from human urine, xanthurenic acid 8-O-␤-D-glucoside and xanthurenic acid 8-O-sulfate. The two compounds were partially purified by activity-guided fractionation and subsequently identified by using NMR spectroscopic analyses of enriched active fractions. Both compounds caused substantial and sustained (1-to 2-h) natriuresis in rats and no or minimal concomitant potassium excretion. We believe these compounds constitute a class of kidney hormones that also could influence sodium transport in nonkidney tissues given that these tryptophan metabolites presumably represent evolutionarily old structures.diuresis ͉ kidney ͉ nonpeptidic ͉ sodium homeostasis ͉ NMR spectroscopy

show abstract

“…Both are heat stable and resist' refrigeration at -80'C. Both inhibit transcellular sodium transport by the urinary bladder of the toad (2,6), when added to the serosal surface but neither affects sodium transport when added to the mucosal surface (2,6). Finally, both are inactivated by leucine amino peptidase (7,8).…”

mentioning

confidence: 99%

The Presence of a Natriuretic Factor in Urine of Patients with Chronic Uremia. THE ABSENCE OF THE FACTOR IN NEPHROTIC UREMIC PATIENTS

Bourgoignie¹,

Hwang²,

Ipakchi³

et al. 1974

J. Clin. Invest.

Self Cite

View full text Add to dashboard Cite

A B S T R A C T A gel filtration fraction of serum from chronically uremic patients has been shown previously to produce natriuresis in the rat. In the present studies, the same fraction from urine of uremic patients and normal subjects was studied for its natriuretic activity. Urine samples were obtained from 17 chronically uremic patients (mean glomerular filtration rate [GFR], 8.7 ml/min; mean fractional sodium excretion [FEN.], 5.7%), and 14 normal subjects. The fraction from the uremic patients produced a significant increase in absolute sodium excretion (UNaV) and FEN.; the fraction from normal subjects had no statistically significant effect on either UNNV or FENa; and the difference between the response to the uremic vs. normal fractions was highly significant for both parameters of sodium excretion. When a more concentrated urine fraction from uremic patients was administered, a striking natriuresis was observed with values for FEN. rising to levels as high as 12%. Studies also were performed on eight patients with far advanced chronic renal insufficiency and the nephrotic syndrome. The serum fraction was studied in each of these patients and the urine fraction in three. For the group, UNaV in the assay rats decreased by 0.87 iueq/min and FENa decreased by 1.35% after infusion of the serum fraction. These results differ significantly from those of patients with chronic uremia without the nephrotic syndrome. The data are consistent with the Parts of this work have been published in abstracted forms (7,8).Dr. Bourgoignie is a recipient of a U. S. Public Health Service Research Career Development Award 7 KO 4 HL 40977.Received for publication 2 October 1973 and in revised form 21 January 1974. view that the increased activity of the natriuretic factor in the serum of chronically uremic patients is not due to failure of excretion; rather it relates either to an increased rate of production and/or a decreased rate of degradation. The data also show that the inhibitor is detectable when FENa is increased, but not when uremia is associated with a sodium-retaining state.

show abstract

The Effects of the Natriuretic Factor from Uremic Urine on Sodium Transport, Water and Electrolyte Content, and Pyruvate Oxidation by the Isolated Toad Bladder

Cited by 31 publications

References 12 publications

An inhibitor of sodium transport in the urine of dogs with normal renal function.

An inhibitor of sodium transport in the urine of dogs with normal renal function.

Identification of xanthurenic acid 8- O -β- d -glucoside and xanthurenic acid 8- O -sulfate as human natriuretic hormones

The Presence of a Natriuretic Factor in Urine of Patients with Chronic Uremia. THE ABSENCE OF THE FACTOR IN NEPHROTIC UREMIC PATIENTS

Contact Info

Product

Resources

About