Ontogeny of cortical collecting duct sodium transport

1994 ◽  
Vol 267 (1) ◽  
pp. F49-F54 ◽  
Author(s):  
V. M. Vehaskari
Keyword(s):  
Active Transport ◽  
Collecting Duct ◽  
Age Groups ◽  
Cortical Collecting Duct ◽  
Na Transport ◽  
Passive Permeability ◽  
Postnatal Maturation ◽  
Two Stages

The postnatal maturation of Na transport in the rabbit cortical collecting duct (CCD) was investigated. CCD segments from rabbits of three different age groups (3-9 days, 10-15 days, and 22-27 days) were perfused in vitro. Lumen-to-bath 22Na fluxes were 38.5 +/- 4.7, 17.0 +/- 2.9, and 30.2 +/- 4.0 pmol.mm-1.min-1 in the three groups, respectively. The high flux in the youngest group was explained by a high passive flux (28.3 +/- 4.2 pmol.mm-1.min-1) determined in the presence of ouabain; the passive 22Na flux in the two other groups (7.1 +/- 2.6 and 3.1 +/- 2.4 pmol.mm-1.min-1) was not significantly different from previously reported adult values. Ouabain-sensitive 22Na flux, reflecting active transport, was low in the two younger groups (10.3 +/- 2.5 and 9.9 +/- 1.9 pmol.mm-1.min-1), but exhibited a rapid increase to 27.1 +/- 2.6 pmol.mm-1.min-1 by 22-27 days of age. In vivo glucocorticoid pretreatment did not affect the Na transport in any age group. Mineralocorticoid pretreatment for 2 days had no effect in the two younger groups, but increased lumen-to-bath 22Na flux from 30.2 +/- 4.0 to 51.1 +/- 4.3 pmol.mm-1.min-1 in the 22- to 27-day-old group. The findings demonstrate that the maturation of rabbit CCD Na transport occurs in two stages, with the first consisting of a decrease in passive permeability during the first 2 wk of life, followed by an increase in active transport and simultaneous development of mineralocorticoid responsiveness.

Cellular actions of cAMP on HCO3(-)-secreting cells of rabbit CCD: dependence on in vivo acid-base status

1994 ◽  
Vol 266 (4) ◽  
pp. F528-F535 ◽  
Author(s):  
C. Emmons ◽  
J. B. Stokes
Keyword(s):  
Anion Exchanger ◽  
Collecting Duct ◽  
Basolateral Membrane ◽  
Disulfonic Acid ◽  
Intercalated Cells ◽  
Cortical Collecting Duct ◽  
Acid Base ◽  
Acid Base Status

HCO3- secretion by cortical collecting duct (CCD) occurs via beta-intercalated cells. In vitro CCD HCO3- secretion is modulated by both the in vivo acid-base status of the animal and by adenosine 3',5'-cyclic monophosphate (cAMP). To investigate the mechanism of cAMP-induced HCO3- secretion, we measured intracellular pH (pHi) of individual beta-intercalated cells of CCDs dissected from alkali-loaded rabbits perfused in vitro. beta-Intercalated cells were identified by demonstrating the presence of an apical anion exchanger (cell alkalinization in response to removal of lumen Cl-). After 180 min of perfusion to permit decrease of endogenous cAMP, acute addition of 0.1 mM 8-bromo-cAMP or 1 microM isoproterenol to the bath caused a transient cellular alkalinization (> 0.20 pH units). In the symmetrical absence of either Na+, HCO3-, or Cl-, cAMP produced no change in pHi. Basolateral dihydrogen 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (0.1 mM) for 15 min before cAMP addition also prevented this alkalinization. In contrast to the response of cells from alkali-loaded rabbits, addition of basolateral cAMP to CCDs dissected from normal rabbits resulted in an acidification of beta-intercalated cells (approximately 0.20 pH units). The present studies demonstrate the importance of the in vivo acid-base status of the animal in the regulation of CCD HCO3- secretion by beta-intercalated cells. The results identify the possible existence of a previously unrecognized Na(+)-dependent Cl-/HCO3- exchanger on the basolateral membrane of beta-intercalated cells in alkali-loaded rabbits.

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)

scholarly journals TRPV4 as a flow sensor in flow-dependent K+ secretion from the cortical collecting duct

2007 ◽  
Vol 292 (2) ◽  
pp. F667-F673 ◽  
Author(s):  
Junichi Taniguchi ◽  
Shuichi Tsuruoka ◽  
Atsuko Mizuno ◽  
Jun-ichi Sato ◽  
Akio Fujimura ◽  
...  
Keyword(s):  
Collecting Duct ◽  
Basolateral Membrane ◽  
Cortical Collecting Duct ◽  
Urine Production ◽  
K Secretion ◽  
Distal Tubules ◽  
Transient Receptor

The transient receptor vanilloid-4 (TRPV4) is a mechanosensitive, swell-activated cation channel that is abundant in the renal distal tubules. Immunolocalization studies, however, present conflicting data as to whether TRPV4 is expressed along the apical and/or basolateral membranes. To disclose the role of TRPV4 in flow-dependent K+ secretion in distal tubules in vivo, urinary K+ excretion and net transports of K+ and Na+ in the cortical collecting duct (CCD) were measured with an in vitro microperfusion technique in TRPV4 +/+ and TRPV4 −/− mice. Both net K+ secretion and Na+ reabsorption were flow dependently increased in the CCDs isolated from TRPV4 +/+mice, which were significantly enhanced by a luminal application of 50 μM 4α-phorbol-12,13-didecanoate (4αPDD), an agonist of TRPV4. No flow dependence of net K+ and Na+ transports or effects of 4αPDD on CCDs were observed in TRPV4 −/− mice. A basolateral application of 4αPDD had little effect on these ion transports in the TRPV4 +/+ CCDs, while the luminal application did. Urinary K+ excretion was significantly smaller in TRPV4 −/− than in TRPV4 +/+ mice when urine production was stimulated by a venous application of furosemide. These observations suggested an essential role of the TRPV4 channels in the luminal or basolateral membrane as flow sensors in the mechanism underlying the flow-dependent K+ secretion in mouse CCDs.

Luminal prostaglandin E2 modulates sodium and water transport in rabbit cortical collecting ducts

1995 ◽  
Vol 268 (6) ◽  
pp. F1093-F1101 ◽  
Author(s):  
Y. Ando ◽  
Y. Asano
Keyword(s):  
Prostaglandin E2 ◽  
Collecting Duct ◽  
Dependent Manner ◽  
Cortical Collecting Duct ◽  
Osmotic Water ◽  
Basolateral Side ◽  
Luminal Side ◽  
Transepithelial Voltage

We have previously found that arginine vasopressin (AVP) acts not only from the basolateral side but also from the luminal side of the rabbit cortical collecting duct (CCD). In the present study, we examined whether prostaglandin E2 (PGE2), another classic and potent modulator of the collecting duct functions, exerts luminal actions in the rabbit CCD perfused in vitro. Although luminal prostaglandin I2 was inert, luminal PGE2 (> 1 nM) induced transient hyperpolarization of transepithelial voltage followed by sustained depolarization in a dose-dependent manner. This action was preserved in the presence of basolateral PGE2, luminal AVP, or luminal BaCl2, but abolished by basolateral ouabain or luminal amiloride. Furthermore, unlike luminal AVP, luminal PGE2 suppressed Na transport and increased osmotic water permeability. The present study suggests that PGE2, similar to AVP but in a different fashion, modulates transepithelial transports from both luminal and basolateral sites in the CCD in vivo.

Sodium and water transport in cortical collecting duct of Dahl salt-resistant rat

1994 ◽  
Vol 267 (4) ◽  
pp. F583-F591 ◽  
Author(s):  
L. H. Kudo ◽  
C. T. Hawk ◽  
J. A. Schafer
Keyword(s):  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Osmotic Water Permeability ◽  
Sprague Dawley ◽  
Osmotic Water ◽  
Depot Injection ◽  
Transepithelial Voltage ◽  
Net Fluxes

Studies were conducted to determine whether the cortical collecting duct (CCD) of the Dahl salt-resistant rat (inbred Rapp strain; R/Jr) exhibits the same responses to deoxycorticosterone (DOC; 2.5 mg as a depot injection in vivo, 3-8 days before experimentation) and arginine vasopressin (AVP, 220 pM in vitro) as the Sprague-Dawley (SD) [L. Chen, S.K. Williams, and J.A. Schafer. Am. J. Physiol. 259 (Renal Fluid Electrolyte Physiol. 28): F147-F156, 1990] and Dahl salt-sensitive (inbred Rapp strain, S/Jr) [C.T. Hawk and J.A. Schafer. Am. J. Physiol. 260 (Renal Fluid Electrolyte Physiol. 29): F471-F478, 1991] CCD. Qualitatively, the R/Jr CCD responded as in the other two strains: AVP elevated the osmotic water permeability (Pf, micron/s) from 0 to approximately 1,200; either AVP or DOC, when used alone, increased the lumen-to-bath 22Na+ flux (Jl-->b, pmol.min-1.mm-1) from the control range of 20-25 to approximately 40 and hyperpolarized the transepithelial voltage. AVP and DOC effects were synergistic, elevating Jl-->b to 90 +/- 5 (mean +/- SE) with both hormones, but this value was significantly lower than observed previously in both the SD and the S/Jr CCD, 125 +/- 6 and 140 +/- 6, respectively. However, bath-to-lumen fluxes (Jb--l) were also significantly lower than observed in the SD and S/Jr CCD. Because net fluxes (Jnet) in these experiments can be determined only as nonpaired differences between unidirectional fluxes, it is uncertain whether Jnet values in the R/Jr CCD are significantly lower than in the SD or S/Jr CCD.(ABSTRACT TRUNCATED AT 250 WORDS)

HCO3- transport in rat CCD: rapid adaptation by in vivo but not in vitro alkalosis

1993 ◽  
Vol 264 (3) ◽  
pp. F435-F440
Author(s):  
J. D. Gifford ◽  
M. W. Ware ◽  
R. G. Luke ◽  
J. H. Galla
Keyword(s):  
Collecting Duct ◽  
Total Carbon ◽  
Cortical Collecting Duct ◽  
Rapid Adaptation ◽  
Acid Base Balance ◽  
Similar Time ◽  
Arterial Ph ◽  
Base Balance

Acute chloride-depletion alkalosis (CDA) in vivo results in sustained net total carbon dioxide (tCO2) secretion in vitro in the rat cortical collecting duct (CCD) for several hours. To determine whether altering in vitro pH and electrolytes similarly result in tCO2 secretion, CCD were incubated for 1 h at 37 degrees C in an alkalotic environment similar to in vivo arterial pH, PCO2, and electrolytes (pH 7.6, 40 mM HCO3). The in vitro alkalosis incubation had no effect on tCO2 transport. Second, alteration of the magnitude of vivo alkalosis was correlated with in vitro tCO2 transport. After generation of CDA by intraperitoneal dialysis against 154 mM HCO3-, rats received an infusion for 2.5 h of either 5% dextrose to maintain alkalosis or 154 mM NaCl at differing rates to partially correct or fully correct the systemic alkalosis. After in vitro isolation and perfusion, in vitro tCO2 flux correlated with in vivo Cl- balance (r2 = 0.82), serum HCO3- (r2 = 0.84), and arterial H+ concentration (r2 = 0.78), but not with K+ balance (r2 = 0.33). These findings suggest that: 1) the regulation of tCO2 transport in vitro correlates with the degree of systemic alkalosis and Cl- balance in vivo, and 2) simulating alkalotic pH and electrolytes in vitro does not rapidly alter transport as does in vivo CDA within a similar time. Taken together, pH and electrolyte changes alone cannot account for the rapid adaptation of tCO2 transport in the CCD, but an in vivo factor(s) contributes importantly to alter tCO2 transport in magnitude and direction that would tend to restore normal acid-base balance.

Functional development of active sugar transport in the chick intestine

1964 ◽  
Vol 207 (1) ◽  
pp. 37-41 ◽  
Author(s):  
Phyllis Holt Bogner ◽  
I. Ann Haines
Keyword(s):  
Active Transport ◽  
Age Groups ◽  
Sugar Transport ◽  
Mutual Inhibition ◽  
Tissue Water ◽  
Functional Development ◽  
Active Transport Process ◽  
Accumulation Method

The intestinal sugar transport function of late embryos and young chicks was studied by means of the tissue-accumulation method. Penetration of intestinal slices by sorbose was minimal in all age groups, ranging between 0.2 and 6.0 µmoles/g dry wt. The ratio of sorbose concentration in tissue water to that in the final medium (T/M) never exceeded 0.3. Galactose uptake by embryonic intestine was comparable to that for sorbose. In contrast, 0-day-old slices accumulated 29 µmoles galactose/g dry wt. which gave a T/M of 3.7. Maximal concentrative power was exhibited by 2-day-old slices which accumulated 38 µmoles galactose/g dry wt., resulting in a T/M of 7.4. Mutual inhibition of active transport between glucose and galactose was observed in 2-day-old slices. In intact chicks alimentary absorption rates of these two sugars rose sharply and to about the same extent between 0 and 2 days of age. Hence both in vitro and in vivo evidence suggests that an active transport process for sugars becomes functional in the chick intestine during the hatching period.

Effect of vasopressin on Na+-K+-ATPase activity in rat cortical collecting duct

1987 ◽  
Vol 253 (5) ◽  
pp. F874-F879 ◽  
Author(s):  
K. Tomita ◽  
A. Owada ◽  
Y. Iino ◽  
N. Yoshiyama ◽  
T. Shiigai
Keyword(s):  
Atpase Activity ◽  
Time Course ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Henle's Loop ◽  
K Secretion ◽  
Medullary Collecting Duct ◽  
Hydrolysis Of

Vasopressin (V) causes a sustained increase in Na reabsorption and K secretion in isolated cortical collecting ducts (CCD) from rats. Because increased Na reabsorption may be associated with increased Na+-K+-ATPase activity, we investigated effects of V, given either in vivo or in vitro, on Na+-K+-ATPase activity in isolated nephron segments of rats. Na+-K+-ATPase activities were measured by coupling the hydrolysis of ATP to the production of a fluorescent nucleotide. In addition to CCD, other microdissected structures were medullary thick ascending limbs of Henle's loop, cortical thick ascending limbs of Henle's loop, and outer medullary collecting duct. To determine the time course of the response, Na+-K+-ATPase activities were measured in CCD 1 h, 3 h, 1 day, 3 days, and 7 days after intramuscular administrations of V. There was a significant increase in Na+-K+-ATPase activity in CCD after in vivo V administration for 7 days but not in any other segment. The activities increased after 3 days of administration of V. For in vitro experiments, CCD were incubated with 10(-6) M V for 1-3 h. Na+-K+-ATPase activities did not change after 1- or 3-h exposure of V in CCD in vitro. We conclude that prolonged V administration in vivo increases Na+-K+-ATPase activity in CCD. Because, in vitro exposure to V does not increase Na+-K+-ATPase activity, we conclude that rapid V-dependent increases in Na and K transport previously demonstrated in isolated perfused tubules are not dependent on a change in maximal Na+-K+-ATPase activity.

scholarly journals Angiotensin II and Renal Tubular Ion Transport

2005 ◽  
Vol 5 ◽  
pp. 680-690 ◽  
Author(s):  
Patricia Valles ◽  
Jan Wysocki ◽  
Daniel Batlle
Keyword(s):  
Angiotensin Ii ◽  
Atpase Activity ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Water Excretion ◽  
Bicarbonate Reabsorption ◽  
Sodium Dependent ◽  
Collecting Tubule

Angiotensin II, a potent vasoconstrictor, also participates in the regulation of renal sodium and water excretion, not only via a myriad of effects on renal hemodynamics, glomerular filtration rate, and regulation of aldosterone secretion, but also via direct effects on renal tubule transport. In addition, angiotensin II stimulates H+secretion and HCO3–reabsorption in both proximal and distal tubules and regulates H+-ATPase activity in intercalated cells of the collecting tubule. Different results regarding the effect of angiotensin II on bicarbonate reabsorption and proton secretion have been reported at the functional level, depending on the angiotensin II concentration and tubule segment studied. It is likely that interstitial angiotensin II is more important in regulating hemodynamic and transport functions than circulating angiotensin II. In proximal tubules, stimulation of bicarbonate reabsorption, Na+/H+-exchange, and Na+/HCO3–cotransport has been found using low concentrations (<10–9M), while inhibition of bicarbonate reabsorption has been documented using concentrations higher than 10–8M. Evidence for the regulation of H+-ATPase activityin vivoandin vitroby trafficking/exocytosis has been provided. An additional level of H+-ATPase regulation via protein synthesis may be important as well. Recently, we have shown that both aldosterone and angiotensin II provide such a mechanism of regulationin vivoat the level of the medullary collecting tubule. Interestingly, in this part of the nephron, the effects of aldosterone and angiotensin II are not sodium dependent, whereas in the cortical collecting duct, both aldosterone and angiotensin II, by contrast, affect H+secretion by sodium-dependent mechanisms.

Mineralocorticoid effects on Na-K-ATPase in individual nephron segments

1981 ◽  
Vol 240 (6) ◽  
pp. F536-F544 ◽  
Author(s):  
L. C. Garg ◽  
M. A. Knepper ◽  
M. B. Burg
Keyword(s):  
Atpase Activity ◽  
Collecting Duct ◽  
Cortical Collecting Duct ◽  
Na Transport ◽  
Nephron Segments ◽  
Low Sodium Diet ◽  
Low Sodium ◽  
Collecting Ducts ◽  
Convoluted Tubules

A fluorometric micromethod for the assay of Na-K-ATPase was used to determine Na-K-ATPase activity in 11 segments of the rabbit nephron. The Na-K-ATPase activity was found to be highest (greater than 100 pmol.mm1-.min-1) in proximal convoluted tubules (S1), medullary thick ascending limbs, distal convoluted tubules, and connecting tubules. There was a good correlation (r = 0.94) between Na-K-ATPase activity in different segments and net Na transport previously measured by in vitro tubule perfusion. Treatment of rabbits with deoxycorticosterone (DOCA) for 8-11 days produced increases in Na-K-ATPase activity of 100 and 500% in connecting tubules and cortical collecting ducts, respectively, without significant change in other segments. Maintenance on a low sodium diet for 12-18 days was associated with a 200% increase in Na-K-ATPase activity in cortical collecting ducts only. We conclude that the Na-K-ATPase activity is stimulated by mineralocorticoids in the cortical collecting duct in association with the previously observed changes in sodium transport.

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