Renal tubular secretion of o-acetylaminohippurate

1962 ◽  
Vol 203 (5) ◽  
pp. 881-885 ◽  
Author(s):  
Gilbert H. Mudge ◽  
Keith Garlid ◽  
I. M. Weiner
Keyword(s):  
Tubular Secretion ◽  
Rabbit Kidney ◽  
Kidney Cortex ◽  
Renal Tubular Secretion ◽  
Kidney Slices ◽  
Tubular Transport ◽  
Clearance Studies ◽  
Renal Tubular Transport ◽  
Renal Tubular

Renal tubular transport of o-acetylaminohippurate (OAAH) was investigated because of previous reports that it differed from other hippurates by not undergoing tubular secretion. However, tubular secretion was readily demonstrable in nine clearance experiments in dogs. Secretion was decreased by succinate, 2,4 DNP, probenecid, hippurate, and Diodrast, substances all known to inhibit secretion of other hippurates. In vivo deacetylation was demonstrated. In slice system of rabbit kidney cortex, accumulation was also shown, but degree of uptake was complicated by deacetylation to OAH. Meta and para isomers did not undergo deacetylation. Both in clearance studies and in kidney slices, the transport of OAAH is qualitatively similar to other hippurates.

The use of mammalian cortical kidney slices for the study of tubule secretion: a pioneering step toward understanding organic anion transport

2006 ◽  
Vol 290 (1) ◽  
pp. F1-F3 ◽  
Author(s):  
William H. Dantzler
Keyword(s):  
Organic Anion ◽  
Anion Transport ◽  
Rabbit Kidney ◽  
Historical Significance ◽  
Kidney Slices ◽  
Tubular Transport ◽  
On Line ◽  
Renal Tubular Transport ◽  
Renal Tubular ◽  
Classic Paper

This essay examines the historical significance of an APS classic paper that is freely available on line: Cross RJ and Taggart JV. Renal tubular transport: accumulation of p-aminohippurate by rabbit kidney slices. Am J Physiol 161: 181–190, 1950 ( http://ajplegacy.physiology.org/cgi/reprint/161/1/181 ).

AVP-stimulated nucleotide secretion in perfused mouse medullary thick ascending limb and cortical collecting duct

2009 ◽  
Vol 297 (2) ◽  
pp. F341-F349 ◽  
Author(s):  
Elvin Odgaard ◽  
Helle A. Praetorius ◽  
Jens Leipziger
Keyword(s):  
Collecting Duct ◽  
Tubular Secretion ◽  
Hormonal Control ◽  
Similar Response ◽  
Thick Ascending Limb ◽  
Cortical Collecting Duct ◽  
Medullary Thick Ascending Limb ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Renal Tubular

Extracellular nucleotides are local, short-lived signaling molecules that inhibit renal tubular transport via both luminal and basolateral P2 receptors. Apparently, the renal epithelium itself is able to release nucleotides. The mechanism and circumstances under which nucleotide release is stimulated remain elusive. Here, we investigate the phenomenon of nucleotide secretion in intact, perfused mouse medullary thick ascending limb (mTAL) and cortical collecting duct (CCD). The nucleotide secretion was monitored by a biosensor adapted to register nucleotides in the tubular outflow. Intracellular Ca2+ concentration ([Ca2+]i) was measured simultaneously in the biosensor cells and the renal tubule with fluo 4. We were able to identify spontaneous tubular nucleotide secretion in resting perfused mTAL. In this preparation, 10 nM AVP and 1-desamino-8-d-arginine vasopressin (dDAVP) induced robust [Ca2+]i oscillations, whereas AVP in the CCD induced large, slow, and transient [Ca2+]i elevations. Importantly, we identify that AVP/dDAVP triggers tubular secretion of nucleotides in the mTAL. After addition of AVP/dDAVP, the biosensor registered bursts of nucleotides in the tubular perfusate, corresponding to a tubular nucleotide concentration of ∼0.2–0.3 μM. A very similar response was observed after AVP stimulation of CCDs. Thus AVP stimulated tubular secretion of nucleotides in a burst-like pattern with peak tubular nucleotide concentrations in the low-micromolar range. We speculate that local nucleotide signaling is an intrinsic feedback element of hormonal control of renal tubular transport.

Renal tubular transport and metabolism of organic cations by the rabbit

1981 ◽  
Vol 241 (3) ◽  
pp. F308-F314 ◽  
Author(s):  
K. Besseghir ◽  
L. B. Pearce ◽  
B. Rennick
Keyword(s):  
Rabbit Kidney ◽  
Organic Cations ◽  
Striking Difference ◽  
Clearance Ratio ◽  
Renal Metabolism ◽  
Future Studies ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Intact Rabbit ◽  
Renal Tubular

The renal tubular transport of the organic cations tetraethylammonium (TEA), N1-methylnicotinamide (NMN), and choline was studied in anesthetized rabbits by the urinary clearance technique. The clearance ratio of [14C]TEA/inulin was 5.72 +/- 0.44 and the clearance ratio of [14C]TEA/p-aminohippuric acid (PAH) was 0.98 +/- 0.02. The clearance ratio of the 14C label/inulin when [14C]NMN was being infused was only 1.31. The clearance ratio of choline/inulin was less than 1 at choline infusion loads from 0 to about 6 mumol . kg-1 . min-1, which produced a plasma choline level of 100 microM. At higher infusion rates the urinary clearance ratio of choline/inulin rose to a maximum of 2 at plasma choline levels of 300–500 microM. Renal metabolism of choline and NMN were revealed by the use of the isolated perfused rabbit kidney. [14C]Choline was extensively metabolized by the kidney into betaine. The renal metabolite of [14C]NMN comigrated with nicotinamide in electrophoresis. The relatively low urinary clearance of the label associated with NMN in the rabbit presents a striking difference from its transport in dog and rat. Studies using isolated perfused segments are done using tissue from rabbits primarily. These data from the intact rabbit kidney may be used to guide future studies of organic cation transport with isolated perfused segments.

scholarly journals Roles of Akt and SGK1 in the Regulation of Renal Tubular Transport

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Nobuhiko Satoh ◽  
Motonobu Nakamura ◽  
Masashi Suzuki ◽  
Atsushi Suzuki ◽  
George Seki ◽  
...  
Keyword(s):  
Proximal Tubules ◽  
Kidney Cortex ◽  
Sodium Reabsorption ◽  
Serine Threonine Kinase ◽  
Akt Phosphorylation ◽  
Renal Transporters ◽  
Collecting Ducts ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
Renal Tubular

A serine/threonine kinase Akt is a key mediator in various signaling pathways including regulation of renal tubular transport. In proximal tubules, Akt mediates insulin signaling via insulin receptor substrate 2 (IRS2) and stimulates sodium-bicarbonate cotransporter (NBCe1), resulting in increased sodium reabsorption. In insulin resistance, the IRS2 in kidney cortex is exceptionally preserved and may mediate the stimulatory effect of insulin on NBCe1 to cause hypertension in diabetes via sodium retention. Likewise, in distal convoluted tubules and cortical collecting ducts, insulin-induced Akt phosphorylation mediates several hormonal signals to enhance sodium-chloride cotransporter (NCC) and epithelial sodium channel (ENaC) activities, resulting in increased sodium reabsorption. Serum- and glucocorticoid-inducible kinase 1 (SGK1) mediates aldosterone signaling. Insulin can stimulate SGK1 to exert various effects on renal transporters. In renal cortical collecting ducts, SGK1 regulates the expression level of ENaC through inhibition of its degradation. In addition, SGK1 and Akt cooperatively regulate potassium secretion by renal outer medullary potassium channel (ROMK). Moreover, sodium-proton exchanger 3 (NHE3) in proximal tubules is possibly activated by SGK1. This review focuses on recent advances in understanding of the roles of Akt and SGK1 in the regulation of renal tubular transport.

Effect of drugs that alter uric acid excretion in man on uric acid clearance in the chicken

1960 ◽  
Vol 198 (3) ◽  
pp. 575-580 ◽  
Author(s):  
Lawrence Berger ◽  
T'sai Fan Yü ◽  
Alexander B. Gutman
Keyword(s):  
Uric Acid ◽  
Tubular Secretion ◽  
Acid Excretion ◽  
Uric Acid Excretion ◽  
Acid Clearance ◽  
Uric Acid Clearance ◽  
Tubular Transport ◽  
Renal Tubular Transport ◽  
The Mean ◽  
Renal Tubular

In 43 chickens, the mean Cinulin was 4.7 ± 1.8 ml/min. (1.8 ± 0.8 ml/kg/min.), mean Curate 29.0 ± 14.9 ml/min. (11.3 ± 6.0 ml/kg/min.) and mean Turate 1.30 ± 0.69 mg/min. (0.48 ± 0.24 mg/kg/min.). Tubular secretion accounted for a mean of 81% of the total urinary urate. Probenecid, sulfinpyrazone, zoxazolamine and high dosages of phenylbutazone, all uricosuric in man, reduced urate excretion in the chicken, apparently by suppressing tubular secretion of urate; CPAH also was reduced. Salicylate, in doses uricosuric in man, had no effect on chicken urate excretion. Pyrazinamide and sodium r-lactate, agents which decrease urate excretion in man, did not alter urate excretion in the chicken. PAH loading experiments demonstrated that as TPAH increased, Turate decreased. These latter findings suggest competition of urate and PAH for renal tubular transport in the chicken.

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