In a recent study it was found that in Mg loaded rats, the fraction of filtered Mg (% E Mg) recovered in the bend of the loop of Henle of papilla was greater than the filtered load. However, the site of this Mg addition was unspecified and could be either the juxtamedullary proximal tubule, the pars recta, or in the papilla, the descending limb of the loop of Henle. In order to investigate the movement of Mg in the various structures of the papilla, we have studied: 1. The transport of this electrolyte along the collecting duct. 2. Its relative concentration in the loop of Henle and in the adjacent vasa recta. The experiments have been performed in hydropenic and Mg loaded rats. In the collecting duct, the inulin and Mg concentrations increase proportionally, indicating an absence of any transport of Mg along this part of this nephron. In the vasa recta of the accessible papilla, the capillary over peripheral plasma Mg ratio (C/UF Mg) in hydropenia and after Mg loading [1.88 +/- 0.15 (ES) and 2.89 +/- 0.25] were significantly lower than the corresponding TF/UF Mg in the adjacent loops of Henle (2.90 +/- 0.17 and 4.04 +/- 0.37). This finding reduces the possibilities of a Mg passive diffusion from the capillaries to the tubular lumen, unless the electrical potential of the descending limb is more negative than -5 mV. The hypothesis of an active secretion, or a passive diffusion of Mg in the deep proximal tubule, in the pars recta, or in the early non accessible descending limb constitutes the other alternative.
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http://dx.doi.org/10.1007/BF00580829 | DOI Listing |
Background: The thin descending limb (DTL) of the loop of Henle is crucial for urine concentration, as it facilitates passive water reabsorption. Despite its importance, little is known about how DTL cells form during kidney development. Single-cell RNA sequencing (scRNA-seq) studies have not definitively identified DTL cells in the developing mouse kidney.
View Article and Find Full Text PDFJ Am Soc Nephrol
January 2025
Centre de Recherche des Cordeliers, INSERM, Sorbonne Université, Université Paris Cité, F-75006 Paris, France.
The renal tubule and collecting duct express a large number of proteins, all having putative immunoreactive motives. Therefore, all can be the target of pathogenic autoantibodies. However, autoimmune tubulopathies seem to be rare and we hypothesize that they are underdiagnosed.
View Article and Find Full Text PDFFront Physiol
December 2024
Department of Internal Medicine, Hypertension and Vascular Research Division, Henry ford hospital, Detroit, MI, United States.
Purpose Of Review: The thick ascending limb (TAL) of loop of Henle is essential for NaCl, calcium and magnesium homeostasis, pH balance and for urine concentration. NKCC2 is the main transporter for NaCl reabsorption in the TAL and its regulation is very complex. There have been recent advancements toward understanding how NKCC2 is regulated by protein trafficking, protein-protein interaction, and phosphorylation/dephosphorylation.
View Article and Find Full Text PDFInt J Mol Sci
December 2024
Department of Pharmacology, National Institute of Cardiology Ignacio Chávez, Juan Badiano No. 1, Col. Seccion XVI, Tlalpan, Mexico City 14080, Mexico.
Chronic hyperglycemia results in morphological and functional alterations of the kidney and microvascular damage, leading to diabetic nephropathy (DN). Since DN progresses to irreversible renal damage, it is important to elucidate a pharmacological strategy aimed for treating DN in the early stage. Here, we used the type 2 diabetic rat model to induce DN and show a nephroprotective effect following the stimulation of PPAR-α, which stabilized renal tight junction components claudin-2, claudin-5, and claudin-16.
View Article and Find Full Text PDFAm J Hypertens
December 2024
Department of Physiology & Biophysics, Cardiovascular-Renal Research Center, Cardiorenal, and Metabolic Diseases Research Center, University of Mississippi Medical Center, Jackson, MS 39216 USA.
Background: Increased circulating bilirubin attenuates angiotensin (Ang) II-induced hypertension and improves renal hemodynamics. However, the intrarenal mechanisms that mediate these effects are not known. The goal of the present study was to test the hypothesis that bilirubin generation in the renal medulla plays a protective role against Ang II-induced hypertension.
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