Phosphate transport in the light segment of the rabbit cortical collecting tubule

1982 ◽  
Vol 242 (4) ◽  
pp. F379-F384
Author(s):  
G. R. Shareghi ◽  
Z. S. Agus
Keyword(s):  
Flow Rate ◽  
Collecting Duct ◽  
Phosphate Transport ◽  
Phosphate Concentration ◽  
Cortical Collecting Duct ◽  
Concentration Gradients ◽  
Collecting Tubule ◽  
Residual Transport ◽  
The Difference ◽  
Rabbit Cortical Collecting Tubule

The mode and mechanism of phosphate transport in the light portion of the rabbit cortical collecting duct were studied with isolated tubular perfusion. Control studies (n = 48) revealed a mean transepithelial potential difference (PD) of -16.5 +/- 1.3 mV and net phosphate absorption (JPO4) of 0.58 +/- 0.07 pmol.mm-1.min-1. To characterize transport, the effects of flow rate, ouabain, amiloride, and phosphate concentration, and parathyroid hormone (PTH) were analyzed. There was a significant linear relationship between JPO4 and flow rate (n = 48) (r = 0.71, P less than 0.025). Increasing the difference between lumen and bath phosphate concentration from -8.0 to +8.0 mg/dl was associated with a stepwise increase in JPO4 from -0.18 +/- 0.02 to 0.93 +/- 0.05 pmol.mm-1.min-1. PTH had no effect on JPO4. To assess the effects of PD, the tubules were treated with either amiloride (n = 6) or ouabain (n = 7). JPO4 fell significant in both circumstances with reduction of PD, although there remained significant residual transport following amiloride addition. The data demonstrate significant phosphate transport in this segment that is independent of PTH and altered by transepithelial electrical and concentration gradients as well as flow rate.

Phosphate transport by isolated rabbit cortical collecting tubule

1980 ◽  
Vol 238 (5) ◽  
pp. F358-F362
Author(s):  
R. A. Peraino ◽  
W. N. Suki
Keyword(s):  
Specific Activity ◽  
Collecting Duct ◽  
Phosphate Transport ◽  
Cortical Collecting Duct ◽  
Renal Handling ◽  
Bathing Medium ◽  
Collecting Tubule ◽  
Absorptive Flux ◽  
Cortical Collecting Tubule

Renal handling of phosphate occurs in the proximal convoluted tubule. Absorption of this anion also occurs in the pars recta and distal convoluted tubule, the latter a structurally and functionally diverse segment. The purpose of the present investigation was to examine phosphate transport by the cortical collecting duct of the rabbit. Segments of cortical collecting tubule, beyond the last cortical branch, were isolated and perfused in vitro with an artificial solution simulating plasma as the perfusing and bathing medium. The perfusion solution contained either 3 or 25 mM bicarbonate. Net phosphate transport was measured using 32P as the radionuclide tracer, with identical specific activity in perfusing and bathing solutions. A net absorptive flux for phosphate was demonstrated, amounting to 2-3% of the delivered load. In addition, this absorptive flux was linearly related to perfusion rate and, thus, delivered load, but independent of the lumen bicarbonate concentration or pH.

Two modes of phosphate transport by turtle urinary bladder

1980 ◽  
Vol 238 (1) ◽  
pp. F31-F36 ◽  
Author(s):  
J. P. Johnson ◽  
S. Green ◽  
J. H. Schwartz
Keyword(s):  
Urinary Bladder ◽  
Phosphate Transport ◽  
Phosphate Concentration ◽  
Acidic Ph ◽  
Alkaline Ph ◽  
The Difference

The effects of changes in pH and addition of CO2/HCO3- on transepithelial phosphate transport were studied in turtle urinary bladder. Net mucosa-to-serosa flux of phosphate (JP) was determined as the difference between unidirectional 32P fluxes in the absence of transepithelial electrochemical gradients. With 5 mM phosphate in HCO3--free Ringer at pH 8.4, JP was 21.8 +/- 7.4 nmol . 8 cm-2 . h-1. There was a slight increase in JP with isohydric addition of 10 mM HCO3-. Addition of 5% CO2, which reduced pH to 7.3, did not affect JP. At pH 8.4, JP was not affected by ouabain or dinitrophenol and increased progressively as phosphate concentration was raised between 0.5 and 10 mM. At pH 6.2 in the absence of exogenous CO2 and HCO3-, JP was undectable. With 2.5 mM HCO3- and 5% CO2 at pH 6.5, JP was 61.3 +/- 16.0 and decreased to 30.6 +/- 1.6 nmol . 8 cm-2 . h-1 when pH was raised to 7.2 by increasing HCO3- to 10 mM. At pH 6.5 JP was inhibited by both ouabain and dinitrophenol. These results suggest that at acidic pH, JP results from the tranport of H2PO4-. The transport of H2PO4- is CO2 dependent and inhibited by ouabain and dinitrophenol. In contrast, at alkaline pH, JP results from the transport of HPO4(2-), which is neither CO2 dependent nor inhibited by ouabain or dinitrophenol.

Cortical collecting duct Na-K pump in obstructive nephropathy

1990 ◽  
Vol 258 (5) ◽  
pp. F1320-F1327 ◽  
Author(s):  
H. Kimura ◽  
S. K. Mujais
Keyword(s):  
Ureteral Obstruction ◽  
Turnover Rate ◽  
Collecting Duct ◽  
Obstructive Nephropathy ◽  
Cortical Collecting Duct ◽  
Sprague Dawley ◽  
Irreversible Damage ◽  
Sprague Dawley Rats ◽  
Collecting Tubule

The present study examined the alterations in the cortical collecting tubule (CCT) Na-K pump that occur after unilateral ureteral obstruction and their consequences on electrolyte excretion. In male Sprague-Dawley rats, unilateral ureteral ligation led to a progressive decrease in intact CCT Na-K pump in situ turnover worsening with the duration of the obstruction: control, 20.1 +/- 0.4; obstructed kidney: 3 h, 14.6 +/- 0.3; 12 h, 12.7 +/- 0.6; 24 h, 12.8 +/- 0.5; 48 h, 11.6 +/- 0.5; and 96 h, 10.6 +/- 0.4 pmol Rb.mm-1.min-1 (all P less than 0.001 vs. control). CCT diameter increased with the duration of obstruction. Release of ureteral obstruction was associated with restitution of pump turnover rate. With 3 h of obstruction, recovery of pump in situ turnover was complete (19.7 +/- 0.4 pmol Rb.mm-1.min-1) by 24 h after release. With more prolonged obstruction (24 h) recovery was partial by 24 h postrelease (16.2 +/- 0.5 pmol Rb.mm-1.min-1) and complete (19.8 +/- 0.7 pmol Rb.mm-1.min-1) by 48 h, suggesting a delay in recovery without the occurrence of irreversible damage. The impairment in Na-K pump in situ turnover was paralleled by an impairment in the ability of the obstructed kidney to excrete an acute potassium load. This parallelism of functional and biochemical studies favors the notion that impairment of CCT Na-K pump in situ turnover contributes significantly to the abnormal potassium excretion that accompanies obstructive damage.

Evidence of corticosteroid action along the nephron

1984 ◽  
Vol 246 (2) ◽  
pp. F111-F123 ◽  
Author(s):  
D. Marver
Keyword(s):  
Collecting Duct ◽  
Type I ◽  
Type Ii ◽  
Cortical Collecting Duct ◽  
Distal Nephron ◽  
Type Iii ◽  
Collecting Ducts ◽  
Collecting Tubule ◽  
Cortical Collecting Tubule

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.

scholarly journals Mechanoregulation of BK channel activity in the mammalian cortical collecting duct: role of protein kinases A and C

2009 ◽  
Vol 297 (4) ◽  
pp. F904-F915 ◽  
Author(s):  
Wen Liu ◽  
Yuan Wei ◽  
Peng Sun ◽  
Wen-Hui Wang ◽  
Thomas R. Kleyman ◽  
...  
Keyword(s):  
Flow Rate ◽  
Collecting Duct ◽  
Bk Channel ◽  
Slow Flow ◽  
Cortical Collecting Duct ◽  
Flow Rates ◽  
Calphostin C ◽  
Flow Stimulation ◽  
Slow Flow Rate ◽  
Stimulation Of

Flow-stimulated net K secretion ( JK) in the cortical collecting duct (CCD) is mediated by an iberiotoxin (IBX)-sensitive BK channel, and requires an increase in intracellular Ca2+ concentration ([Ca2+]i). The α-subunit of the reconstituted BK channel is phosphorylated by PKA and PKC. To test whether the BK channel in the native CCD is regulated by these kinases, JK and net Na absorption ( JNa) were measured at slow (∼1) and fast (∼5 nl·min−1·mm−1) flow rates in rabbit CCDs microperfused in the presence of mPKI, an inhibitor of PKA; calphostin C, which inhibits diacylglycerol binding proteins, including PKC; or bisindolylmaleimide (BIM) and Gö6976, inhibitors of classic and novel PKC isoforms, added to luminal (L) and/or basolateral (B) solutions. L but not B mPKI increased JK in CCDs perfused at a slow flow rate; a subsequent increase in flow rate augmented JK modestly. B mPKI alone or with L inhibitor abolished flow stimulation of JK. Similarly, L calphostin C increased JK in CCDs perfused at slow flow rates, as did calphostin C in both L and B solutions. The observation that IBX inhibited the L mPKI- and calphostin C-mediated increases in JK at slow flow rates implicated the BK channel in this K flux, a notion suggested by patch-clamp analysis of principal cells. The kinase inhibited by calphostin C was not PKC as L and/or B BIM and Gö6976 failed to enhance JK at the slow flow rate. However, addition of these PKC inhibitors to the B solution alone or with L inhibitor blocked flow stimulation of JK. Interpretation of these results in light of the effects of these inhibitors on the flow-induced elevation of [Ca2+]i suggests that the principal cell apical BK channel is tonically inhibited by PKA and that flow stimulation of JK in the CCD is PKA and PKC dependent. The specific targets of the kinases remain to be identified.

Postnatal maturation of potassium transport in rabbit cortical collecting duct

1994 ◽  
Vol 266 (1) ◽  
pp. F57-F65 ◽  
Author(s):  
L. M. Satlin
Keyword(s):  
Flow Rate ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Flow Rates ◽  
Postnatal Maturation ◽  
Significant Linear Correlation ◽  
Potassium Secretion ◽  
Tubular Flow ◽  
Neonatal Kidney

Clearance studies in newborns demonstrate low rates of urinary excretion of potassium, suggesting that the neonatal kidney contributes to the conservation of potassium necessary for growth. Because the cortical collecting duct (CCD) is a primary site for potassium secretion in the adult, we sought to examine the transport capacity of this segment for potassium during postnatal maturation. CCDs isolated from rabbits of various ages (5-6 animals/age group) were microperfused in vitro with solutions simulating plasma. The concentrations of potassium in samples of collected fluid, measured by helium glow photometry, were used to calculate net transport. At a flow rate of approximately 1.6 nl.min-1 x mm-1 net potassium secretion was absent at birth, first became evident at 4 wk of age (-11.08 +/- 2.39 pmol.min-1 x mm-1), and increased sharply thereafter to reach mature rates (-23.08 +/- 3.47 pmol.min-1 x mm-1; P < 0.05) by 6 wk of age. To determine whether low distal tubular flow rates limit net potassium secretion in the neonate, we perfused CCDs at two or more flow rates in the 0.5–5 nl.min-1 x mm-1 range. In CCDs taken from animals > or = 6 wk of age, potassium secretion showed a significant linear correlation with flow rate (y = -10.0x - 7.45; r = 0.87; n = 12).(ABSTRACT TRUNCATED AT 250 WORDS)

1,25(OH)2D3 binding along the rat nephron: autoradiographic study in isolated tubular segments

1985 ◽  
Vol 248 (2) ◽  
pp. F296-F307 ◽  
Author(s):  
C. Manillier ◽  
N. Farman ◽  
J. P. Bonjour ◽  
J. P. Bonvalet
Keyword(s):  
Binding Sites ◽  
Specific Binding ◽  
Collecting Duct ◽  
Distal Tubule ◽  
Autoradiographic Study ◽  
Cortical Collecting Duct ◽  
Dihydroxyvitamin D3 ◽  
Collecting Tubule ◽  
Autoradiographic Technique

1,25-dihydroxyvitamin D3 [1,25(OH)2D3] binding sites were studied along the nephron of rats. The animals were pretreated with the diphosphonate EHDP at doses that inhibit the endogenous production of 1,25(OH)2D3. A dry film autoradiographic technique was applied to tubular segments isolated by microdissection from kidneys incubated in vitro with various concentrations (0.2-12 nM) of [3H]1,25(OH)2D3 in the presence or absence of an excess unlabeled hormone (X200) in order to determine specific binding. Total, nonspecific, and specific labeling were quantified by silver grain counting over cytoplasmic and nuclear areas. Specific nuclear labeling appeared in the cortical ascending limb and papillary collecting tubule at 1 nM. In the distal tubule and, to a lesser extent, in the cortical collecting tubule a specific nuclear labeling was also present, but only at higher concentrations. No specific nuclear labeling was detected in the proximal tubule. All along the nephron, a significant and nonspecific labeling was observed in the cytoplasm, either alone or superimposed over the specific nuclear labeling. In conclusion 1,25(OH)2D3 specific binding sites appear to be localized mainly in the cortical ascending limb of the loop of Henle, in the distal and cortical collecting duct, and in the papillary collecting duct.

scholarly journals An unexpected journey: conceptual evolution of mechanoregulated potassium transport in the distal nephron

2016 ◽  
Vol 310 (4) ◽  
pp. C243-C259 ◽  
Author(s):  
Rolando Carrisoza-Gaytan ◽  
Marcelo D. Carattino ◽  
Thomas R. Kleyman ◽  
Lisa M. Satlin
Keyword(s):  
Flow Rate ◽  
Fluid Shear Stress ◽  
Collecting Duct ◽  
Critical Role ◽  
Bk Channels ◽  
Bk Channel ◽  
Macromolecular Complex ◽  
Urinary Flow ◽  
Cortical Collecting Duct ◽  
Distal Nephron

Flow-induced K secretion (FIKS) in the aldosterone-sensitive distal nephron (ASDN) is mediated by large-conductance, Ca2+/stretch-activated BK channels composed of pore-forming α-subunits (BKα) and accessory β-subunits. This channel also plays a critical role in the renal adaptation to dietary K loading. Within the ASDN, the cortical collecting duct (CCD) is a major site for the final renal regulation of K homeostasis. Principal cells in the ASDN possess a single apical cilium whereas the surfaces of adjacent intercalated cells, devoid of cilia, are decorated with abundant microvilli and microplicae. Increases in tubular (urinary) flow rate, induced by volume expansion, diuretics, or a high K diet, subject CCD cells to hydrodynamic forces (fluid shear stress, circumferential stretch, and drag/torque on apical cilia and presumably microvilli/microplicae) that are transduced into increases in principal (PC) and intercalated (IC) cell cytoplasmic Ca2+ concentration that activate apical voltage-, stretch- and Ca2+-activated BK channels, which mediate FIKS. This review summarizes studies by ourselves and others that have led to the evolving picture that the BK channel is localized in a macromolecular complex at the apical membrane, composed of mechanosensitive apical Ca2+ channels and a variety of kinases/phosphatases as well as other signaling molecules anchored to the cytoskeleton, and that an increase in tubular fluid flow rate leads to IC- and PC-specific responses determined, in large part, by the cell-specific composition of the BK channels.

What is responsible for the diurnal variation in potassium excretion?

1994 ◽  
Vol 267 (2) ◽  
pp. R554-R560 ◽  
Author(s):  
A. Steele ◽  
H. deVeber ◽  
S. E. Quaggin ◽  
A. Scheich ◽  
J. Ethier ◽  
...  
Keyword(s):  
Diurnal Variation ◽  
Flow Rate ◽  
Concentration Gradient ◽  
Potassium Concentration ◽  
Excretion Rate ◽  
Collecting Duct ◽  
Potassium Excretion ◽  
Cortical Collecting Duct ◽  
Diurnal Pattern ◽  
K Concentration

Potassium excretion exhibits a diurnal pattern, with most excretion occurring close to noon in humans. Each component of the K+ excretion rate [urinary K+ concentration ([K+]) and flow rate] was measured and back-calculated to reflect events in the cortical collecting duct (CCD). Our purpose was to determine to what extent each component contributed to this diurnal variation in each 2-h portion of the day. In humans, K+ excretion rose threefold from nadir (0600 h) to peak (1200-1400 h), 18 h after the principal intake of K+. The variation in K+ excretion was due almost exclusively to changes in [K+] in the terminal CCD ([K+]CCD) rather than via changes in flow rate. In rats, the bulk of K+ excretion occurred shortly after eating. Both components of K+ excretion rose after meals; the rise in the [K+]CCD (3.3-fold) predominated at earlier times, and the rise in flow rate occurred later and was primarily a result of a higher rate of excretion of urea. The rise in [K+]CCD did not correlate with aldosterone levels or administration. A very large rise in the [K+]CCD only occurred in the presence of bicarbonaturia; the transtubular potassium concentration gradient was now close to 15 in the morning and evening.

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