Renal transport sites for K, H and NH3. Effect of impermeant anions on their transport

1960 ◽  
Vol 198 (2) ◽  
pp. 244-254 ◽  
Author(s):  
Lawrence P. Sullivan ◽  
Walter S. Wilde ◽  
Richard L. Malvin
Keyword(s):  
Negative Charge ◽  
Distal Tubule ◽  
Sodium Reabsorption ◽  
Renal Transport ◽  
Transport Mechanisms ◽  
Collecting Ducts ◽  
Tubular Lumen ◽  
Potassium Hydrogen ◽  
A Site ◽  
Stop Flow

The stop flow technique was used to locate the sites of the renal transport mechanisms for potassium, hydrogen and ammonium. Data were obtained which indicate that these cations are secreted in a very distal area of the nephron, presumably in the collecting ducts. Potassium reabsorption also occurs in a distal area immediately proximal to the secretory site. Infusions of thiosulfate, ferrocyanide and phosphate alter the stop flow concentration patterns so that secretion of the cations appears to take place throughout the distal tubule and to be coextensive with distal sodium reabsorption. No clear indication of potassium reabsorption is evident under these circumstances. It is suggested that these anions, because of the impermeability of the distal tubule to them and because of their negative charge, attract hydrogen and potassium into the tubular lumen as sodium is reabsorbed. In effect, an abnormal exchange mechanism is created at a site proximal to that where active secretion of hydrogen and potassium occurs.

Stop-flow analysis applied to the excretion of hemoglobin

1960 ◽  
Vol 199 (2) ◽  
pp. 292-294 ◽  
Author(s):  
C. L. Malmendier ◽  
J. P. DeKoster ◽  
F. Vander Veiken ◽  
H. Brauman ◽  
M. DeMyttenaere ◽  
...  
Keyword(s):  
Flow Analysis ◽  
Middle Part ◽  
The Other ◽  
Physiological Data ◽  
Sodium Reabsorption ◽  
Water Reabsorption ◽  
Tubular Lumen ◽  
Influence Of Water ◽  
Stop Flow ◽  
Ureteral Occlusion

The stop-flow analysis has been applied to the study of the excretion of hemoglobin, in order to compare the physiological data with the morphological views. The study of the ratio U/P hemoglobin/U/P creatinine suggests that this protein penetrates the tubular lumen by diffusion during the ureteral occlusion and progressed slowly under influence of water reabsorption. During this migration, hemoglobin undergoes the effects of a double reabsorption: one in the middle part of the proximal convoluted tubule, the other more distally situated in a zone not distinguishable from the site of sodium reabsorption.

Localization of Acidification of Urine, Potassium and Ammonia Secretion and Phosphate Reabsorption in the Nephron of the Dog

1958 ◽  
Vol 194 (1) ◽  
pp. 125-134 ◽  
Author(s):  
Robert F. Pitts ◽  
Ruth S. Gurd ◽  
Richard H. Kessler ◽  
Klaus Hierholzer
Keyword(s):  
Distal Part ◽  
Potassium Phosphate ◽  
Proximal Part ◽  
Ammonium Ion ◽  
Sodium Reabsorption ◽  
Hydrogen Ions ◽  
Acid Urine ◽  
Urine Potassium ◽  
A Site ◽  
Stop Flow

The Malvin, Sullivan and Wilde ( The Physiologist 1: 58, 1957) stop flow technique for the localization of tubular function has been applied to a study of potassium and acid excretion in the dog. It has been observed that the urine is acidified in the distal part of the nephron at a site of avid sodium reabsorption. Potassium and ammonia are secreted in the same portion of the tubule. Diamox reduces acidification of the urine and secretion of ammonia and enhances the secretion of potassium. Phosphate is reabsorbed in the proximal part of the nephron in a region which is coextensive with that which secretes p-aminohippurate. All our data are consonant with the view that a mechanism located in the distal part of the nephron exchanges cellular hydrogen and/or potassium ions for sodium ions in the tubular urine. Ammonia diffuses into acid urine and is trapped as ammonium ion. Diamox, by interfering with the supply of cellular hydrogen ions, reduces exchange of hydrogen for sodium and favors the exchange of potassium for sodium.

Site of reabsorption of citrate and calcium in the renal tubule of the dog

1963 ◽  
Vol 205 (4) ◽  
pp. 697-701 ◽  
Author(s):  
Arthur P. Grollman ◽  
W. Gordon Walker ◽  
Helen C. Harrison ◽  
Harold E. Harrison
Keyword(s):  
Distal Tubule ◽  
Renal Tissue ◽  
Distal Region ◽  
Proximal Region ◽  
Sodium Reabsorption ◽  
Sodium Potassium ◽  
Tissue Samples ◽  
Calcium Reabsorption ◽  
Stop Flow ◽  
Edta Infusion

Simultaneous reabsorptive patterns of calcium, citrate, sodium, potassium, creatinine, and para-aminohippurate (PAH) were determined by stop-flow technique during the infusion of calcium chloride and the neutral sodium salts of malate, citrate, and ethylenediaminetetraacetate (EDTA). Citrate reabsorption during citrate infusion occurred in the proximal nephron, coinciding with the area of PAH secretion while the calcium reabsorptive minimum was in the distal tubule, coinciding with the pattern of sodium reabsorption. Malate infusion abolishes citrate reabsorption, stimulates the distal secretion of potassium and, despite the marked increase in citrate excretion, fails to increase citrate concentration in renal tissue samples. EDTA infusion obliterates the calcium reabsorption minimum without affecting the more proximal pattern of citrate reabsorption. It is concluded that maximum citrate reabsorption occurs in the proximal region of the nephron distinctly separate from the more distal region of maximum calcium reabsorption.

Stop-flow analysis of the influence of pCO2 on renal tubular transport of K and H

1964 ◽  
Vol 206 (6) ◽  
pp. 1355-1360 ◽  
Author(s):  
A. G. Ramsay
Keyword(s):  
Flow Analysis ◽  
Distal Tubule ◽  
Respiratory Alkalosis ◽  
Reciprocal Relationship ◽  
Tubular Transport ◽  
K Secretion ◽  
Renal Tubular Transport ◽  
Renal Tubular ◽  
A Site ◽  
Stop Flow

The stop-flow procedure was used to study the transport of H and K ions in the renal tubule during conditions of high and low pCO2. The increased rate of K excretion during respiratory alkalosis was due primarily to marked increase of K secretion at a distal site. The interrupted stop flow showed that K reabsorption was decreased at a site just proximal to the secretory area. This made a smaller contribution to the increased K excretion. The reciprocal relationship between tubular transport of K and H was demonstrable. CO2 tension appeared to influence HCO3 reabsorption and H secretion in both the distal and proximal tubule, whereas its effect on K transport was confined to the distal tubule. Hypercapnia never completely obliterated the distal secretory site. It is suggested that a pCO2-dependent H carrier is not shared with K. The increased K secretion of hypocapnia is more likely the result of increased K within the distal tubular cells.

Physical Properties of Isolated Perfused Renal Tubular Basement Membranes

1971 ◽  
Vol 29 ◽  
pp. 390-391
Author(s):  
Jared Grantham ◽  
Larry Welling
Keyword(s):  
Basement Membrane ◽  
Basement Membranes ◽  
Transport Mechanisms ◽  
Permeability Characteristics ◽  
Peritubular Capillaries ◽  
Strategic Location ◽  
Tubular Lumen ◽  
Glomerular Filtrate ◽  
Urine Formation ◽  
Renal Tubular

In the course of urine formation in mammalian kidneys over 90% of the glomerular filtrate moves from the tubular lumen into the peritubular capillaries by both active and passive transport mechanisms. In all of the morphologically distinct segments of the renal tubule, e.g. proximal tubule, loop of Henle and distal nephron, the tubular absorbate passes through a basement membrane which rests against the basilar surface of the epithelial cells. The basement membrane is in a strategic location to affect the geometry of the tubules and to influence the movement of tubular absorbate into the renal interstitium. In the present studies we have determined directly some of the mechanical and permeability characteristics of tubular basement membranes.

Downregulation of renal TonEBP in hypokalemic rats

2007 ◽  
Vol 293 (1) ◽  
pp. F408-F415 ◽  
Author(s):  
Un Sil Jeon ◽  
Ki-Hwan Han ◽  
Soo-Hyun Park ◽  
Sang Do Lee ◽  
Mee Rie Sheen ◽  
...  
Keyword(s):  
Cultured Cells ◽  
Renal Medulla ◽  
Distal Tubule ◽  
Cell Type ◽  
Outer Medulla ◽  
Sodium Transporters ◽  
Enhancer Binding Protein ◽  
Collecting Ducts ◽  
Cell Type Specific ◽  
Underlying Mechanisms

Hypokalemia causes a significant decrease in the tonicity of the renal medullary interstitium in association with reduced expression of sodium transporters in the distal tubule. We asked whether hypokalemia caused downregulation of the tonicity-responsive enhancer binding protein (TonEBP) transcriptional activator in the renal medulla due to the reduced tonicity. We found that the abundance of TonEBP decreased significantly in the outer and inner medullas of hypokalemic rats. Underlying mechanisms appeared different in the two regions because the abundance of TonEBP mRNA was lower in the outer medulla but unchanged in the inner medulla. Immunohistochemical examination of TonEBP revealed cell type-specific differences. TonEBP expression decreased dramatically in the outer and inner medullary collecting ducts, thick ascending limbs, and interstitial cells. In the descending and ascending thin limbs, TonEBP abundance decreased modestly. In the outer medulla, TonEBP shifted to the cytoplasm in the descending thin limbs. As expected, transcription of aldose reductase, a target of TonEBP, was decreased since the abundance of mRNA and protein was reduced. Downregulation of TonEBP appeared to have also contributed to reduced expression of aquaporin-2 and UT-A urea transporters in the renal medulla. In cultured cells, expression and activity of TonEBP were not affected by reduced potassium concentrations in the medium. These data support the view that medullary tonicity regulates expression and nuclear distribution of TonEBP in the renal medulla in cell type-specific manners.

Abstract 360: Increased Aldosterone Sensitivity in Young Blacks

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Wanzhu Tu ◽  
Hai Liu ◽  
George Eckert ◽  
J Howard Pratt
Keyword(s):  
Volume Expansion ◽  
Distal Tubule ◽  
Plasma Renin ◽  
Sodium Reabsorption ◽  
Sodium Retention ◽  
Lower Plasma ◽  
Blacks And Whites ◽  
Small Increments ◽  
Using Data ◽  
Different Levels

Aldosterone contributes to the elevation of blood pressure (BP) by acting on the distal tubule to cause greater sodium retention and volume expansion. Blacks, in comparison with whites, have lower plasma aldosterone concentrations (PAC), possibly due to increased sodium reabsorption and resultant renin suppression, as evidenced by their lower plasma renin activity (PRA); but BP is on average higher in blacks. The seemingly different BP-PAC relationships in blacks and whites raise point to the possibility of different aldosterone sensitivity in the two race groups. Using data from a cohort of normotensive youths (n=654 observations contributed by 537 subjects), we used a varying coefficient model to examine the BP effect of PAC at different levels of PRA in blacks and whites. We characterized the effects of PAC as a function of PRA and assessed its effect on age, sex, and height-adjusted BP percentile. The estimated effects are presented graphically (Figure 1 a&b). Blacks had lower PRA and PAC (PRA: 2.8 vs 3.3, p=0.002; PAC: 8.7 vs 14.1, p<0.0001; PAC/PRA: 4.7 vs 5.4, p=0.172), and marginally higher systolic and diastolic BP percentiles (SBP%: 44.5 vs 40.6, p=0.082; DBP%: 57 vs 51, p=0.004). In blacks, the BP effect of PAC was much greater in blacks at lower PRA levels (p=0.004); in whites, PAC effect on BP was not significant (p=0.164) and the effect did not change noticeably with PRA. In conclusion, the finding supports the notion that blacks have higher levels of aldosterone sensitivity, especially for those with lower PRA. A sustained state of volume expansion appears to make blacks vulnerable to the BP effects of even small increments in sodium retention produced by aldosterone.

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.

Effects of flow rate and potassium intake on distal tubular potassium transfer

1975 ◽  
Vol 228 (4) ◽  
pp. 1249-1261 ◽  
Author(s):  
RN Khuri ◽  
WN Strieder ◽  
G Giebisch
Keyword(s):  
Flow Rate ◽  
Electrical Potential ◽  
Isotonic Saline ◽  
Distal Tubule ◽  
Sodium Reabsorption ◽  
Electrical Potential Difference ◽  
High Potassium ◽  
Flow Rates ◽  
Potassium Intake ◽  
Potassium Secretion

Potassium transport was studied across proximal and distal tubular epithelium in rats on a normal, low- and high-potassium intake during progressive loading with isotonic saline (150 mM) or a moderately hypersomotic urea (200 mM) sodium chloride (100 mM) solution. Free-flow micropuncture and recollection techniques were used during the development of diruesis and tubular fluid (TF) analyzed for inulin-14C, potassium (K) and sodium (Na). Tubular puncture sites were localized by neoprene filling and microdissection. During the large increase in tubular flow rates (10 times): 1) fractional potassium reabsorption fell along the proximal tubule, 2) TFk along the distal tubule remained constant and independent of flow rate in control and high-k rats; thus, net potassium secretion increased in proportion to and was limited by flow rate. 3) In low-K rats TF k fell; with increasing flow rates distal K secretion was not effectively stimulated. 4) Distal tubular sodium reabsorption increased in all animals with flow rate, but tubular Na-K exchange ratios varied greatly. It is suggested that whenever sodium delivery stimulates distal tubular potassium secretion it does so by 1) increasing volume distal tubular potasssium secretion and by 2) augmenting the transepithelial electrical potential difference (lumen negative).

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