To determine the relative importance of plasma and luminal pH changes as factors regulating potassium secretion by rat distal tubule, superficial tubules were continuously microperfused in vivo. The effects of changes in plasma pH were examined by producing acute systemic metabolic acidosis or alkalosis and holding luminal flow rate, solute composition, and pH constant by microperfusion. Alternatively, the effect of luminal solution pH was evaluated by microperfusing tubules with solutions buffered to either pH 6.5 or 8.0 at constant systemic acid-base balance. Net transport of Na and K and the pH of the luminal fluid were measured. Results showed that metabolic acidosis inhibited and metabolic alkalosis stimulated potassium secretion. Increased luminal fluid pH, in contrast, did not stimulate potassium transport. In experiments in which metabolic acidosis produced a diuresis, urinary potassium excretion was enhanced compared with hydropenic controls. Free-flow micropuncture studies revealed that the rate of fluid delivery to the distal tubule was 45% greater during acidosis compared with control and that potassium secretion increased in both the distal and collecting tubule. Since the rate of fluid delivery is a potent stimulus of potassium secretion in the distal tubule, it is concluded that the stimulus of increased delivery of fluid, observed in free-flow conditions, masked the inhibitory effect of acidosis on potassium transport. Potassium transport by the distal tubule, during acid-base disorders, is regulated by plasma pH and the rate of delivery of fluid but is not stimulated by alkalinization of the luminal fluid.
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http://dx.doi.org/10.1152/ajprenal.1982.242.5.F544 | DOI Listing |
Kidney360
December 2024
Department of Internal Medicine, Division of Nephrology and Transplantation, Erasmus Medical Center, University Medical Center Rotterdam, Rotterdam, the Netherlands.
Background: Epidermal growth factor is expressed in the distal tubule and secreted in urine (uEGF) after cleavage of membrane-bound pro-EGF. Lower uEGF is associated with kidney disease progression. EGF also plays a role in the regulation of serum magnesium and blood pressure, but whether uEGF is associated with these parameters is unknown.
View Article and Find Full Text PDFCompr Physiol
December 2024
Division of Nephrology and Hypertension, Department of Medicine, Oregon Health and Science University, Portland, Oregon, USA.
The rare disease Familial Hyperkalemic Hypertension (FHHt) is caused by mutations in the genes encoding Cullin 3 (CUL3), Kelch-Like 3 (KLHL3), and two members of the With-No-Lysine [K] (WNK) kinase family, WNK1 and WNK4. In the kidney, these mutations ultimately cause hyperactivation of NCC along the renal distal convoluted tubule. Hypertension results from increased NaCl retention, and hyperkalemia by impaired K secretion by downstream nephron segments.
View Article and Find Full Text PDFKidney Res Clin Pract
December 2024
Graduate School of International Agricultural Technology, Seoul National University, Pyeongchang, Republic of Korea.
Extracellular vesicles (EVs) are nanosized membranous particles released by nearly all cell types, playing a crucial role in mediating cell-to-cell communication. The molecular profile of EVs often reflects that of their originating cells, rendering them valuable for therapeutic and diagnostic purposes. The kidney comprises various cell types, and urinary EVs are predominantly produced from tubular, glomerular, and urinary bladder cells.
View Article and Find Full Text PDFJ Mol Histol
December 2024
Department of Morphology, Federal University of Rio Grande do Norte, Natal, Brazil.
Diabetic nephropathy (DN) is one of the most relevant and prevalent microvascular complications associated with Diabetes Mellitus. In recent years, hyperbaric oxygen therapy (HBO) has been used to mitigate tissue damage caused by hypoxia, thereby attenuating inflammatory processes. This study aimed to explore morphological aspects associated with DN in rats subjected to HBO.
View Article and Find Full Text PDFPresse Med
December 2024
Division of Pathology, Hôpital Maisonneuve-Rosemont, Université de Montréal, Montréal, Canada.
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