SGK1: A Rapid Aldosterone-Induced Regulator of Renal Sodium Reabsorption

Physiology ◽  
2005 ◽  
Vol 20 (2) ◽  
pp. 134-139 ◽  
Author(s):  
James A. McCormick ◽  
Vivek Bhalla ◽  
Alan C. Pao ◽  
David Pearce
Keyword(s):  
Knockout Mice ◽  
Cultured Cells ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Important Mediator ◽  
Physiological Relevance ◽  
Tight Epithelia ◽  
Substantial Progress ◽  
Renal Sodium Reabsorption ◽  
Made In

Recently, substantial progress has been made in understanding the mechanisms by which aldosterone rapidly stimulates sodium transport in the distal nephron and other tight epithelia. Serum- and glucocorticoid-regulated kinase 1 (SGK1) has been identified as an important mediator of this process. Its physiological relevance has been revealed through heterologous expression in cultured cells and generation of SGK1 knockout mice.

Renal sodium reabsorption following induction of recovery from volume expansion

1977 ◽  
Vol 233 (5) ◽  
pp. F416-F420
Author(s):  
T. F. Knight ◽  
E. J. Weinman
Keyword(s):  
Urinary Excretion ◽  
Proximal Tubule ◽  
Volume Expansion ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Recovery Phase ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Renal Sodium Reabsorption ◽  
Distal Delivery

In the rat, infusion of a volume of isotonic saline equal to 2% of body weight resulted in an 82% increase in delivery of filtrate out of the proximal tubule but little or, in some animals, no change in the urinary excretion of sodium. By contrast, further degrees of volume expansion resulted in lesser increases in the distal delivery of filtrate, but were associated with a marked increase in the urinary excretion of sodium. Sixty minutes following completion of volume expansion, while the animals were still in positive sosium balance, the urinary excretion of sodium decreased 52% compared to a decrease of only 24% in the distal delivery of filtrate. During the course of progressive volume expansion and during the recovery phase, there was a dissociation between alterations in sodium reabosrption in the proximal convoluted tubule and in the whole kidney. These studies indicate that although the proximal tubule is more sensitive to changes in the extracellular fluid volume, distal nephron sites are ultimately responsible both for the natriuresis of volume expansion and the relative antinatriuresis of the recovery periods.

Single-nephron function and renal oxygen consumption during rapid volume expansion

1976 ◽  
Vol 231 (4) ◽  
pp. 1166-1172 ◽  
Author(s):  
SW Weinstein ◽  
J Szyjewicz
Keyword(s):  
Oxygen Consumption ◽  
Proximal Tubule ◽  
Volume Expansion ◽  
Ringer Solution ◽  
Sodium Reabsorption ◽  
Distal Nephron ◽  
Renal Oxygen Consumption ◽  
Single Nephron ◽  
Proximal Tubular ◽  
Renal Sodium Reabsorption

Isotonic volume expansion reduces net filtrate reabsorption in the proximal tubule while increasing it in Henle's loop. To determine the role oxidative metabolism plays in these processes, experiments were performed on rats initially hydropenic and then rapidly volume expanded with isotonic Ringer solution. Whole-kidney sodium reabsorption, oxygen consumption, and single-nephron function were measured simultaneously. During volume expansion, net renal sodium reabsorption increased concomitantly with a fall in oxygen consumption and a reduction in proximal tubular absolute filtrate reabsorption. The increase in quantity of nonreabsorbed filtrate delivered into the loop of Henle greatly exceeded the amount excreted in the urine. Thus, filtrate reabsorption by the distal nephron segments increased. These data provide evidence that acute volume expansion reduces oxygen-dependent active solute transport in the proximal tubule. The increase noted in distal nephron sodium reabsorption appears nonoxygen dependent, energized by anaerobic glycolysis or occurring passively.

Insulin Effect on Renal Sodium Reabsorption in Adolescent Offspring of Essential Hypertensive Parents

Hypertension ◽  
1995 ◽  
Vol 26 (6) ◽  
pp. 1089-1092 ◽  
Author(s):  
B. Grunfeld ◽  
M. Gimenez ◽  
M. Balzaretti ◽  
L. Rabinovich ◽  
M. Romo ◽  
...  
Keyword(s):  
Sodium Reabsorption ◽  
Insulin Effect ◽  
Adolescent Offspring ◽  
Renal Sodium Reabsorption

THE STATUS OF TWO-NEUTRINO AND NEUTRINOLESS DOUBLE BETA DECAY SEARCHES

1993 ◽  
Vol 02 (03) ◽  
pp. 507-546 ◽  
Author(s):  
M.K. MOE
Keyword(s):  
Beta Decay ◽  
Neutrinoless Double Beta Decay ◽  
Double Beta Decay ◽  
Experimental Activity ◽  
The Past ◽  
The Status ◽  
Substantial Progress ◽  
Direct Counting ◽  
Made In

Substantial progress has been made in double beta decay experiments in the past few years, including the beginning of sensitive new searches for neutrinoless double beta decay, and several additional positive detections of the two-neutrino mode by geochemical, radiochemical, and direct-counting techniques. This review discusses the recent experimental activity.

Stimulation of renal sodium reabsorption by angiotensin II

1977 ◽  
Vol 232 (4) ◽  
pp. F298-F306 ◽  
Author(s):  
M. D. Johnson ◽  
R. L. Malvin
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Flow Rate ◽  
Sodium Reabsorption ◽  
Urinary Flow ◽  
Filtration Fraction ◽  
Water Diuresis ◽  
Urinary Osmolality ◽  
Anesthetized Dogs ◽  
Renal Sodium Reabsorption

Various parameters of renal function were studied before, during, and after the infusion of physiological increments of angiotensin II directly into one renal artery of anesthetized dogs. During water diuresis and during antidiuresis induced with exogenous antidiuretic hormone (ADH), angiotensin II consistently reduced UNaV, UKV, and CPAH, and increased the filtration fraction in the infused kidney. Urinary osmolality was increased only in the presence of ADH, while during water diuresis angiotensin II had no apparent effect on urinary osmolality or flow rate. During saline diuresis, a mean increment of angiotensin II concentration of 14 pg/ml was sufficient to significantly reduce UNaV and urinary flow rate. Changes in CCr, CPAH, and filtration fraction did not correlate with changes in sodium excretion, and intracortical distribution of blood flow remained unaltered. These data support the hypothesis that normal circulating levels of angiogensin II play a direct renal role in the control of sodium, potassium, and water homeostasis, and that angiotensin II exerts a direct, stimulatory effect on tubular sodium reabsorption independent of changes in GFR, RPF, filtration fraction, or intracortical distribution of blood flow.

scholarly journals Interaction between Epithelial Sodium Channel γ-Subunit and Claudin-8 Modulates Paracellular Sodium Permeability in Renal Collecting Duct

2020 ◽  
Vol 31 (5) ◽  
pp. 1009-1023 ◽  
Author(s):  
Ali Sassi ◽  
Yubao Wang ◽  
Alexandra Chassot ◽  
Olga Komarynets ◽  
Isabelle Roth ◽  
...  
Keyword(s):  
Sodium Channel ◽  
Knockout Mice ◽  
Collecting Duct ◽  
Epithelial Sodium Channel ◽  
Paracellular Permeability ◽  
Sodium Reabsorption ◽  
Kidney Tubule ◽  
Sodium Permeability ◽  
Tubular Lumen ◽  
Renal Collecting Duct

BackgroundWater and solute transport across epithelia can occur via the transcellular or paracellular pathways. Tight junctions play a key role in mediating paracellular ion reabsorption in the kidney. In the renal collecting duct, which is a typical absorptive tight epithelium, coordination between transcellular sodium reabsorption and paracellular permeability may prevent the backflow of reabsorbed sodium to the tubular lumen along a steep electrochemical gradient.MethodsTo investigate whether transcellular sodium transport controls tight-junction composition and paracellular permeability via modulating expression of the transmembrane protein claudin-8, we used cultured mouse cortical collecting duct cells to see how overexpression or silencing of epithelial sodium channel (ENaC) subunits and claudin-8 affect paracellular permeability. We also used conditional kidney tubule–specific knockout mice lacking ENaC subunits to assess the ENaC’s effect on claudin-8 expression.ResultsOverexpression or silencing of the ENaC γ-subunit was associated with parallel and specific changes in claudin-8 abundance. Increased claudin-8 abundance was associated with a reduction in paracellular permeability to sodium, whereas decreased claudin-8 abundance was associated with the opposite effect. Claudin-8 overexpression and silencing reproduced these functional effects on paracellular ion permeability. Conditional kidney tubule–specific ENaC γ-subunit knockout mice displayed decreased claudin-8 expression, confirming the cell culture experiments' findings. Importantly, ENaC β-subunit or α-subunit silencing or kidney tubule–specific β-ENaC or α-ENaC knockout mice did not alter claudin-8 abundance.ConclusionsOur data reveal the specific coupling between ENaC γ-subunit and claudin-8 expression. This coupling may play an important role in preventing the backflow of reabsorbed solutes and water to the tubular lumen, as well as in coupling paracellular and transcellular sodium permeability.

Persistent Questions About The Oxygen Donor In Silicon

1985 ◽  
Vol 59 ◽  
Author(s):  
Michael Stavola
Keyword(s):  
Formation Kinetics ◽  
Oxygen Donor ◽  
Substantial Progress ◽  
Made In

In spite of 30 years of study the most basic questions about the oxygen donor in silicon remain unanswered. There are not accepted models for the structure or formation kinetics. There is not even agreement on what the donor's constituents are. Nonetheless, substantial progress has been made in this field in recent years [1] that narrows model ideas and helps to focus continuing research.

scholarly journals Rings whose additive endomorphisms are ring endomorphisms

1990 ◽  
Vol 42 (1) ◽  
pp. 145-152 ◽  
Author(s):  
Gary Birkenmeier ◽  
Henry Heatherly
Keyword(s):  
Subdirectly Irreducible ◽  
Finiteness Conditions ◽  
Chain Conditions ◽  
Open Questions ◽  
Open Case ◽  
Ring Endomorphism ◽  
Substantial Progress ◽  
Additive Endomorphism ◽  
Made In

A ring R is said to be an AE-ring if every additive endomorphism is a ring endomorphism. In this paper further steps are made toward solving Sullivan's Problem of characterising these rings. The classification of AE-rings with. R3 ≠ 0 is completed. Complete characterisations are given for AE-rings which are either: (i) subdirectly irreducible, (ii) algebras over fields, or (iii) additively indecomposable. Substantial progress is made in classifying AE-rings which are mixed – the last open case – by imposing various finiteness conditions (chain conditions on special ideals, height restricting conditions). Several open questions are posed.

scholarly journals Proximal and Distal Nephron-specific Adaptation to Furosemide

2021 ◽  
Author(s):  
Aram J. Krauson ◽  
Steven Schaffert ◽  
Elisabeth M. Walczak ◽  
Jonathan M. Nizar ◽  
Gwen M. Holdgate ◽  
...  
Keyword(s):  
Cell Number ◽  
Differentially Expressed ◽  
Sodium Reabsorption ◽  
Thick Ascending Limb ◽  
Distal Nephron ◽  
Transcriptional Responses ◽  
Cell Hyperplasia ◽  
Diuretic Resistance ◽  
Nephron Segments ◽  
Renal Tubular

ABSTRACTFurosemide, a widely prescribed diuretic for edema-forming states, inhibits sodium reabsorption in the thick ascending limb of the nephron. Tubular adaptation to diuretics has been observed, but the range of mechanisms along the nephron has not been fully explored. Using morphometry, we show that furosemide induces renal tubular epithelial hyperplasia selectively in distal nephron segments. By comparison, we find progressive cellular hypertrophy in proximal and distal nephron segments. We next utilize single cell RNA sequencing of vehicle- and furosemide-treated mice to define potential mechanisms of diuretic resistance. Consistent with distal tubular cell hyperplasia, we detect a net increase in DCT cell number and Birc5, an anti-apoptotic and pro-growth gene, in a subset of DCT cells, as the most prominently up-regulated gene across the nephron. We also map a gradient of cell-specific transcriptional changes congruent with enhanced distal sodium transport. Furosemide stimulates expression of the mitogen IGF-1. Thus, we developed a mouse model of inducible deletion of renal tubular IGF-1 receptor and show reduced kidney growth and proximal, but not distal, tubular hypertrophy by furosemide. Moreover, genes that promote enhanced bioavailability of IGF-1 including Igfbp1 and Igfbp5 are significantly and differentially expressed in proximal tubular segments and correspond to IGF-1R-dependent hypertrophy. In contrast, downstream PI3-kinase signaling genes including Pdk1, Akt1, Foxo3, FKBP4, Eif2BP4, and Spp1 are significantly and differentially expressed in distal nephron segments and correspond to IGF-1R-independent hypertrophy. These findings highlight novel mechanisms of tubular remodeling and diuretic resistance, provide a repository of transcriptional responses to a common drug, and expand the implications of long-term loop diuretic use for human disease.

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