The collecting tubule of Amphiuma. II. Effects of potassium adaptation

1987 ◽  
Vol 253 (6) ◽  
pp. F1273-F1282 ◽  
Author(s):  
J. D. Horisberger ◽  
M. Hunter ◽  
B. Stanton ◽  
G. Giebisch
Keyword(s):  
Sodium Current ◽  
Apical Cell ◽  
Potassium Conductance ◽  
Transport Pathway ◽  
High Potassium ◽  
Apical Cell Membrane ◽  
High Sodium ◽  
Collecting Tubule ◽  
Potassium Secretion ◽  
Collecting Tubules

Electrophysiological and transport properties were studied in isolated and perfused Amphiuma collecting tubules from two groups of animals, one exposed to a high sodium (NA), the other to a high potassium (KA) environment (both conditions known to modulate blood aldosterone levels). The transepithelial lumen-negative potential was significantly larger (-38 +/- 5 mV) in tubules from KA animals than from NA animals (-15 +/- 3 mV). In addition, we observed an increase in the apical amiloride-sensitive sodium conductance and stimulation of the transepithelial sodium current. Although no measurable potassium conductance was found in the apical cell membrane in either group, a potassium selectivity of the paracellular transport pathway was observed in the KA animals. Net potassium secretion was demonstrated in KA tubules (helium-glow photometry and [3H]inulin analysis). Potassium secretion was abolished by luminal amiloride but imposition of a bath-to-lumen potassium gradient induced potassium secretion. We conclude that in contrast to the mammalian cortical collecting tubule in which potassium secretion is largely transcellular, potassium secretion in the Amphiuma collecting tubule is by diffusion through the paracellular pathway.

The collecting tubule of Amphiuma. I. Electrophysiological characterization

1987 ◽  
Vol 253 (6) ◽  
pp. F1263-F1272 ◽  
Author(s):  
M. Hunter ◽  
J. D. Horisberger ◽  
B. Stanton ◽  
G. Giebisch
Keyword(s):  
Cell Membrane ◽  
Cell Model ◽  
Basolateral Membrane ◽  
Apical Cell ◽  
Potassium Conductance ◽  
Sodium Reabsorption ◽  
Apical Cell Membrane ◽  
Cation Selectivity ◽  
Basolateral Cell Membrane ◽  
Collecting Tubules

Single collecting tubules of Amphiuma kidneys were perfused in vitro to characterize their electrophysiological properties. The lumen-negative potential (-24 mV) was abolished by amiloride in the lumen and by ouabain in the bath. Ion substitution experiments in the lumen demonstrated the presence of a large sodium conductance in the apical cell membrane, but no evidence was obtained for a significant potassium or chloride conductance. Ion substitutions in the bath solution and the depolarizing effect of barium on the basolateral membrane potential demonstrated the presence of a large potassium conductance in the basolateral cell membrane. Measurements of dilution potentials in amiloride-treated tubules revealed a modest cation selectivity of the paracellular pathway. These results support a cell model in which sodium reabsorption occurs by electrodiffusion across the apical cell membrane and active transport across the basolateral cell membrane. The absence of a detectable potassium conductance in the apical cell membrane suggests that secretion of this ion cannot take place by diffusion from cell to lumen.

Ca2(+)-dependent inhibition of sodium transport in rabbit cortical collecting tubules

1990 ◽  
Vol 258 (3) ◽  
pp. F568-F582 ◽  
Author(s):  
G. Frindt ◽  
E. E. Windhager
Keyword(s):  
Cell Membrane ◽  
Amphotericin B ◽  
Apical Cell ◽  
Ringer Solution ◽  
Na Transport ◽  
Apical Cell Membrane ◽  
Dependent Inhibition ◽  
Collecting Tubules ◽  
Rate Limiting ◽  
Sustained Increase

Experiments were carried out to test whether maneuvers believed to increase intracellular Ca2+ concentration [( Ca2+]cell) inhibit Na transport in cortical collecting tubules (CCTs). Unidirectional Na efflux (JNa1----b) and Na influx (JNab----1) were measured isotopically in isolated perfused renal CCTs of rabbits. The animals were either untreated or pretreated with deoxycorticosterone (DOC) for 1-3 wk. To raise [Ca2+]cell, ionomycin or quinidine were added to, or [Na] reduced in, pertubular fluid. In control DOC-pretreated CCTs JNa1----b tended to saturate as luminal Na concentration was increased, reaching 22.9 +/- 1.2 pmol.cm-1.s-1 at 145 mM. In addition, in these CCTs, in contrast to non-DOC-treated tubules, the apical cell membrane was not found to be rate limiting for Na reabsorption as neither amphotericin B nor vasopressin further enhanced JNa1----b. In non-DOC-treated CCTs 10(-6) M ionomycin inhibited JNa1----b by 44.7%. When DOC-pretreated CCTs were exposed to either 10(-6)M ionomycin or 10(-4)M quinidine, JNa1----b was inhibited by 27 and 26%, respectively, while JNab----1 remained unchanged. This ionomycin-induced inhibition was Ca dependent. Exposure of DOC-pretreated CCTs to 5 mM Na-Ringer solution (Na replaced by choline or N-methyl-D-glucamine) for 30 min reduced JNa1----b by 18-30%. The inhibition of JNa1----b caused by any of the three maneuvers was fully reversed upon addition of amphotericin B to the luminal fluid. The results are consistent with the view that a sustained increase in [Ca2+]cell reduces Na transport by inhibition of the rate of Na+ entry across the apical cell membrane.

Cellular organization of urinary acidification

1986 ◽  
Vol 251 (2) ◽  
pp. F173-F187 ◽  
Author(s):  
P. R. Steinmetz
Keyword(s):  
Apical Membrane ◽  
Apical Cell ◽  
Freeze Fracture ◽  
Transport Systems ◽  
Sodium Absorption ◽  
Bicarbonate Secretion ◽  
Transport Pathway ◽  
Apical Cell Membrane ◽  
Membrane Area ◽  
Urinary Acidification

The turtle bladder contains transport systems for active sodium absorption, electrogenic proton secretion, and bicarbonate secretion (coupled to chloride absorption) that are functionally separate and occur in specialized epithelial cells. Maneuvers that alter the intracellular acid-base state, such as changes in PCO2, cause marked changes in the apical membrane area of alpha-type carbonic anhydrase (CA) cells by addition or retrieval of membrane vesicles but have no effect on the granular cells that transport sodium. The apical cell membrane of alpha-CA cells contains characteristic rod-shaped intramembrane particles (RSP) by freeze fracture and is coated on its cytoplasmic side with studs. A subpopulation of CA cells (beta-type), which is characterized by apical microvilli, fails to exhibit an apical response to CO2 stimulation and does not reveal RSPs or studs at its apical membranes; instead, these elements can be demonstrated at the basolateral membrane. The reversal in the polarity of these elements as well as physiological evidence suggest that beta-type cells are responsible for bicarbonate secretion. Structure-function studies of CO2 stimulation of H+ secretion by alpha-CA cells indicate that the secretion rate (JH) correlates with apical membrane area and numbers of RSPs. The view that RSPs represent arrays of transmembrane channels and that studs represent catalytic units of H+ pumps is supported by quantitative considerations but remains to be proven. Urinary acidification is regulated not only by changes in the number of H+ pumps but also by the intrinsic properties of the H+ pump itself. For a given pump population, JH is closely controlled by the delta microH across the active transport pathway.

scholarly journals Sequential tubular cell and basement membrane changes in polycystic kidney disease.

1992 ◽  
Vol 3 (2) ◽  
pp. 244-253
Author(s):  
F A Carone ◽  
S Nakamura ◽  
P Punyarit ◽  
Y S Kanwar ◽  
W J Nelson
Keyword(s):  
Cell Proliferation ◽  
Kidney Disease ◽  
Basement Membrane ◽  
Polycystic Kidney Disease ◽  
Apical Cell ◽  
Renal Cysts ◽  
Polycystic Kidney ◽  
Apical Cell Membrane ◽  
Tubular Cells ◽  
Collecting Tubules

Tubular basement membrane (BM) changes (dysmorphogenesis), cell proliferation, and fluid accumulation related to the altered location of Na,K-ATPase are purported essential key events in the development and progression of renal cysts. These changes were assessed daily in Phenol II (2-amino-4-hydroxyphenyl-5-phenyl thiazole)-treated rats, which rapidly develop marked and progressive cystic change of all collecting tubules (CT). At Day 1, 12% of CT were cystic and their BM were thickened severalfold. At Day 4, 30% of CT were cystic and their BM remained thickened. BM of cystic tubules showed decreased staining for heparan sulfate proteoglycan and increased staining for fibronectin. Proliferation, as determined by (3H)thymidine, incorporation, was not significant until Day 2 and involved cystic and noncystic tubular cells as well as interstitial cells. As cystic changes progressed, cell proliferation decreased. By immunohistochemistry, the altered location of Na,K-ATPase in epithelial cells lining cysts was primarily detected after Day 2 and consisted of focal loss from basal and/or lateral cell membranes and localization in the cell cytoplasm. Only rarely was Na,K-ATPase localized to the apical cell membrane. After the removal of Phenol II, cystic tubular cells, BM, and Na,K-ATPase returned to normal. Thus, in this model of polycystic kidney disease, initial cyst formation occurred in tandem with BM structural change whereas cell proliferation and altered location of Na,K-ATPase occurred after the appearance of cysts.

Ionic conductive properties and electrophysiology of the rabbit cortical collecting tubule

1982 ◽  
Vol 243 (1) ◽  
pp. F81-F95 ◽  
Author(s):  
R. G. O'Neil ◽  
E. L. Boulpaep
Keyword(s):  
Cell Membrane ◽  
Tight Junction ◽  
Apical Cell ◽  
Apical Cell Membrane ◽  
Electrophysiological Properties ◽  
Basolateral Cell Membrane ◽  
Collecting Tubule ◽  
Conductive Properties ◽  
K Permeability ◽  
Cortical Collecting Tubule

The Na, K, and Cl conductive properties and the electrophysiological variability of the rabbit isolated cortical collecting tubule were assessed by evaluating the effect of single-ion substitutions on the transepithelial potential difference, Vte, and the transepithelial conductance, Gte. The Na permeability (and conductance) of the tight junction and basolateral cell membrane appeared to be low. However, a significant but variable amiloride-sensitive Na conductance was identified at the apical cell membrane. Although this Na conductance accounts for less than 10% of the Gte, variations in this conductance caused major alterations in the active transepithelial Na current and the Vte. A highly variable K permeability (and conductance) was also identified at the apical cell border and may account for some of the variability in Vte and Gte. This probably provides a pathway for K secretion from cell to lumen. The K permeability of the tight junction and basolateral cell membrane appeared to be relatively low. In contrast, the Cl permeability (and conductance) of the tight junction, and perhaps of the basolateral cell membrane, appeared to be high but variable and to account for the major fraction of the Gte and its variability. It is concluded that variations in the Na and K conductance of the apical cell membrane and the Cl conductance of the tight junction and basolateral cell membrane predominantly account for the variations in the electrophysiological properties of the cortical collecting tubule.

New pathways for potassium transport in the kidney

1982 ◽  
Vol 242 (4) ◽  
pp. F297-F312 ◽  
Author(s):  
R. L. Jamison ◽  
J. Work ◽  
J. A. Schafer
Keyword(s):  
Mass Flow ◽  
Potassium Concentration ◽  
Collecting Duct ◽  
Potassium Transport ◽  
Thick Ascending Limb ◽  
High Potassium ◽  
Pars Recta ◽  
Potassium Secretion ◽  
Medullary Collecting Duct ◽  
Collecting Tubules

This review focuses on the hypothesis that potassium is recycled in the medulla by secretion into the pars recta or descending limb of long-looped nephrons and reabsorption from the ascending limb and/or medullary collecting duct. Evidence supporting the recycling hypothesis is summarized and the process is analyzed quantitatively by an examination of the mass flow of potassium reaching different sites along superficial and juxtamedullary nephrons and collecting tubules. From differences in potassium mass flow between sites, we have estimated the amount of potassium that must be secreted or absorbed by individual segments of the renal tubule. These rates of secretion and absorption are compared with the potassium transport characteristics of the respective segments, as assessed by isolated tubule perfusion in vitro and micropuncture in vivo. It is apparent that potassium secretion can occur passively in the pars recta and descending limb of long-looped nephrons as a consequence of the elevated potassium concentration in the medullary interstitium. At present, no active potassium absorptive mechanism has been demonstrated in any segment of the ascending limb. Due to the very high ionic permeability of the thin ascending segment and the lumen-positive transepithelial voltage in the thick ascending segment, however, considerable passive absorption likely occurs, although net potassium secretion has also been demonstrated in the cortical thick ascending limb. The high potassium concentration in the inner medullary interstitium and the difference in mass flow of potassium between the end of superficial nephrons in the cortex and the collecting ducts in the papilla, at least under certain circumstances, are best accounted for by net potassium reabsorption in the medullary collecting duct.

Effect of ouabain on K secretion in cortical collecting tubules from adrenalectomized rabbits

1984 ◽  
Vol 247 (4) ◽  
pp. F588-F595 ◽  
Author(s):  
C. S. Wingo
Keyword(s):  
Atpase Activity ◽  
Treated Group ◽  
Complete Inhibition ◽  
Collecting Tubule ◽  
K Secretion ◽  
Potassium Secretion ◽  
Transepithelial Voltage ◽  
Collecting Tubules ◽  
Ouabain Inhibition ◽  
Cortical Collecting Tubule

Previous studies have shown that Na-K-ATPase activity in the cortical collecting tubule of the rabbit increases significantly with mineralocorticoid stimulation and decreases significantly with adrenalectomy. The present study examined the effects of 10(-4) M ouabain on K secretion in the isolated perfused cortical collecting tubules from normal, adrenalectomized, and mineralocorticoid-stimulated animals. Potassium secretion was similar in the tubules from adrenalectomized (3.42 +/- 0.53 pmol X mm-1 X min-1) and from normal rabbits (3.38 +/- 0.36 pmol X mm-1 X min-1). K secretion was greater (15.1 +/- 3.0 pmol X mm-1 X min-1) in tubules from animals receiving 11-deoxycorticosterone acetate (DOCA). Ouabain inhibition of K secretion was 74% for the adrenalectomized group, 86% for the normal group, and 98% for the DOCA-treated group. The degree of inhibition was statistically equivalent among the three groups and not statistically different from complete inhibition of K secretion. Ouabain had no effect on the lumen-positive transepithelial voltage of the cortical collecting tubules from adrenalectomized rabbits but reduced the lumen-negative voltage in tubules from normal rabbits and reversed the polarity of the transepithelial voltage in cortical collecting tubules from DOCA-treated animals. Thus adrenal mineralocorticoids may be necessary for maximal K secretion by the cortical collecting tubule, but they are not essential to maintain K secretion during "normal" K intake. In all groups K secretion is totally dependent on Na-K-ATPase. The lumen-positive transepithelial voltage from DOCA-treated animals after addition of ouabain suggests an additional effect of mineralocorticoid to stimulate secretion of cations (protons) or reabsorption of anions.

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