Role of the Na:K Pump in Potassium Handling by the Distal Nephron: Implications for Renal K Adaptation

Author(s):  
Adrian I. Katz
Keyword(s):  
1999 ◽  
Vol 277 (6) ◽  
pp. F821-F825 ◽  
Author(s):  
Lawrence G. Palmer

K-selective channels in the luminal membranes of distal nephron segments form a key pathway for the secretion of K ions into the urine. This process is important to the control of K balance, particularly under conditions of normal or high K intake. This brief review will cover three issues: 1) the identification of apical K channels, 2) the role of these channels in the maintenance of K homeostasis, and 3) the role of aldosterone in this regulatory process. The large amount of literature on renal K transport has been elegantly summarized in a recent review in this journal [G. Giebisch. Am. J. Physiol.274 ( Renal Physiol. 43): F817–F833, 1998]. Here I will focus on a few prominent unsolved problems.


1984 ◽  
Vol 246 (2) ◽  
pp. F111-F123 ◽  
Author(s):  
D. Marver

The kidney contains three classes of corticosteroid-binding proteins receptors. They include a mineralocorticoid-specific (Type I), a glucocorticoid-specific (Type II), and a corticosterone-specific (Type III) site. The Type I and Type III sites roughly parallel each other along the nephron, with maximal binding occurring in the late distal convoluted or connecting segment and the cortical and medullary collecting ducts. Type II sites occur throughout the nephron, with maximal concentrations appearing in the proximal tubule and the late distal convoluted-cortical collecting duct region. The function of the Type I sites in the connecting segment is unclear since chronic mineralocorticoid therapy does not influence the potential difference in this segment as it does in the cortical collecting tubule. Furthermore, the specific role of Type II versus Type III sites in the distal nephron is unknown. Finally, the possible influence of sodium on both latent and steroid-induced renal cortical and medullary Na-K-ATPase is discussed.


1985 ◽  
Vol 248 (1) ◽  
pp. R93-R98 ◽  
Author(s):  
G. L. Anderson ◽  
E. J. Braun

The role of the cloaca and lower intestine in the postrenal modification of urine was studied in conscious normally hydrated desert quail. The birds were studied for a period of 12 days during which they were in intake-output balance. It was calculated that of the combined mixture of urine-feces entering the lower intestine, 47% water, 62% sodium, and 49% potassium were reabsorbed. If this material is considered as coming from the ureteral urine, then the composition of the ureteral urine entering the lower intestine was changed as follows: 77% water, 72% sodium, and 82% potassium were reabsorbed. For urate, 68% of the total present in ureteral urine was degraded in the lower intestine. In terms of the filtered load produced by the kidneys, the lower intestine reabsorbed 1.5% filtered water, 0.4% filtered sodium, and 46% filtered potassium. The total filtered loads reabsorbed by the combined efforts of the kidney and lower intestine were 99.5% water, 99.8% sodium, and 88% potassium. It appears that the cloaca and lower intestine of birds may serve a similar function to that of the distal nephron in mammals, making the fine adjustments in water and sodium reabsorption from the urine.


1976 ◽  
Vol 230 (3) ◽  
pp. 699-705 ◽  
Author(s):  
UF Michael ◽  
J Kelley ◽  
H Alpert ◽  
CA Vaamonde

Free water clearance (CH2O) was measured during hypotonic saline infusion in Sprague-Dawley and in Brattleboro (DI) rats with 131I-induced hypothyroidism and their age-matched controls. At peak urine flow, which was similar in hypothyroid DI (HDI) and control DI (CDI) rats, inulin clearance (CIn/kg) and CH2O/kg were 23 and 20% (P less than 0.02) lower in HDI. Fractional urine flow and fractional sodium excretion were 30 and 40% (P less than 0.001) higher in HDI. Utilization of distal delivery of filtrate for CH2O, formation was 16% less in HDI (P less than 0.01). Papillary osmolality was not higher in HDI rats. Data in Sprague-Dawley rats were similar to those of the DI rats, indicating that endogenous ADH was effectively suppressed. It is concluded: 1) delivery of filtrate out of the proximal tubule was not diminished in hypothyroid rats in spite of a decrease in CIn; 2) despite a similar delivery of filtrate to the distal diluting site, CH2O formation was less in hypothyroid rats than in controls; 3) these data suggest that a defect in the diluting segment could be unmasked at high rates of filtrate delivered to the distal nephron; 4) this defect could be either due to impaired sodium chloride reabsorption or due to increased backdiffusion of water in the distal nephron.


2014 ◽  
Vol 33 (2) ◽  
pp. 333-343 ◽  
Author(s):  
Juliana Martins da Costa-Pessoa ◽  
Rosélia Santos Damasceno ◽  
Ubiratan Fabres Machado ◽  
Olívia Beloto-Silva ◽  
Maria Oliveira-Souza

2004 ◽  
Vol 286 (6) ◽  
pp. F1063-F1071 ◽  
Author(s):  
Wing Y. Li ◽  
Catherine L. Huey ◽  
Alan S. L. Yu

Claudins are integral membrane proteins of the tight junction that determine the magnitude and selectivity of paracellular permeability in epithelial tissues. The mammalian renal tubule exhibits considerable heterogeneity in the permeability properties of its different segments. To determine the nephron segment localization of claudin-7 and -8, immunofluorescence staining of mouse kidney sections was performed using isoform-specific antibodies. Claudin-8 was found to be expressed primarily at the tight junction along the entire aldosterone-sensitive distal nephron and in the late segments of the thin descending limbs of long-looped nephrons. This pattern of expression is consistent with the putative role of claudin-8 as a paracellular cation barrier. By contrast, claudin-7 was found in the same nephron segments as claudin-8, but it was expressed primarily at the basolateral membrane.


2006 ◽  
Vol 291 (5) ◽  
pp. F923-F931 ◽  
Author(s):  
Lisa M. Satlin ◽  
Marcelo D. Carattino ◽  
Wen Liu ◽  
Thomas R. Kleyman

Thiazide and loop diuretics induce renal K+ secretion, often leading to renal K+ wasting and hypokalemia. This phenomenon has been proposed to reflect an increase in delivery to and reabsorption of Na+ by the distal nephron, with a resultant increase in the driving force for passive K+ efflux across the apical membrane. Recent studies suggest that cellular mechanisms that lead to enhanced rates of Na+ reabsorption as well as K+ secretion in response to increases tubular flow rates are more complex. Increases in tubular flow rates directly enhance the activity of apical membrane Na+ channels and indirectly activate a class of K+ channels, referred to as maxi-K, that are functionally inactive under low flow states. This review addresses the role of biomechanical forces, generated by variations in urinary flow rate and tubular fluid volume, in the regulation of transepithelial Na+ and K+ transport in the distal nephron. The question of why the distal nephron has evolved to include a component of flow-dependent K+ secretion is also addressed.


2011 ◽  
Vol 589 (14) ◽  
pp. 3611-3621 ◽  
Author(s):  
Marc Fila ◽  
Gaëlle Brideau ◽  
Luciana Morla ◽  
Lydie Cheval ◽  
Georges Deschênes ◽  
...  

2005 ◽  
Vol 288 (4) ◽  
pp. F846-F854 ◽  
Author(s):  
Jennifer L. Pluznick ◽  
Peilin Wei ◽  
P. Richard Grimm ◽  
Steven C. Sansom

Large, Ca2+-activated K+ channels (BK), comprised of α- and β-subunits, mediate K+ secretion during high flow rates in distal nephron segments. Because the BK-β1 subunit enhances Ca2+ sensitivity of BK in a variety of cells, we determined its role in flow-induced K+ secretion and its localization in the mammalian nephron. To determine the role of BK-β1 in the kaliuretic response to volume expansion, the rate of K+ excretion (UKV) vs. varied urinary flow rates were determined in wild-type and BK-β1 knockout mice (BK-β1−/−). When flow rate was varied by volume expansion (2 ml·h−1·25 g body wt−1) for 30 to 60 min in wild-type mice, we found that the UKV increased significantly with increasing urine flow rates ( r2 = 0.50, P < 0.00001, n = 31), as demonstrated previously in distal nephron of rats and rabbits. However, in BK-β1−/− mice, UKV did not vary with changing flow rates ( r2 = 0.15, P = 0.08, n = 20). Using immunohistochemical techniques, we found that BK-β1 was strongly expressed in the apical membrane of the murine distal nephron and that 98% of BK-β1 protein detected by histochemistry colocalized with NCX, a marker of connecting tubules (CNT). Both BK-β1 and NCX colocalized with BK-α in separate experiments. Furthermore, we confirmed BK-β1 protein expression in the apical membrane of connecting tubules in rabbits. BK-β1 RNA from rabbit CNT was sequenced and was identical to previously published rabbit muscle sequences. These data show that the BK-β1 accessory subunit is present in the CNT segment of the mammalian distal nephron and has a significant role in the kaliuretic response to increased urinary flow induced by volume expansion.


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