Electrophysiologic study of the cortical collecting tubule of the rabbit

Hanley, Michael; Kokko, Juha P.; Gross, James B.; Jacobson, Howard

doi:10.1038/ki.1980.9

Cited by 26 publications

(11 citation statements)

References 25 publications

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“…A lumen-negative transepithelial voltage exists across isolated cortical collecting ducts (42,43). This lumen-negative voltage is generated by the active sodium transport (42).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Renal Calcium Handling by 11β-Hydroxysteroid Dehydrogenase Type 2

Ferrari

Bianchetti²,

Sansonnens³

et al. 2002

Journal of the American Society of Nephrology

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Abstract. Reduced concentration of serum ionized calcium and increased urinary calcium excretion have been reported in primary aldosteronism and glucocorticoid-treated patients. A reduced activity of the 11␤-hydroxysteroid dehydrogenase type 2 (11␤HSD2) results in overstimulation of the mineralocorticoid receptor by cortisol. Whether inhibition of the 11␤HSD2 by glycyrrhetinic acid (GA) may increase renal calcium excretion is unknown. Serum and urinary electrolyte and creatinine, serum ionized calcium, urinary calcium excretion, and the steroid metabolites (THFϩ5␣THF)/THE as a parameter of 11␤HSD2 activity were repeatedly measured in 20 healthy subjects during baseline conditions and during 1 wk of 500 mg/d GA. One week of GA induced a maximal increment of 93% in (THFϩ5␣THF)/THE. Ambulatory BP was significantly higher at day 7 of GA than at baseline (126/77 Ϯ 10/7 versus 115/73 Ϯ 8/6 mmHg; P Ͻ 0.001 for systolic; P Ͻ 0.05 for diastolic). During GA administration, serum ionized calcium decreased from 1.26 Ϯ 0.05 to 1.18 Ϯ 0.04 mmol/L (P Ͻ 0.0001), and absolute urinary calcium excretion was enhanced from 29.2 Ϯ 3.6 to 31.9 Ϯ 3.1 mol/L GFR (P Ͻ 0.01). Fractional calcium excretion increased from 2.4 Ϯ 0.3 to 2.7 Ϯ 0.3% (P Ͻ 0.01) and was negatively correlated to the fractional sodium excretion during GA (R ϭ Ϫ0.35; P Ͻ 0.001). Moreover, serum potassium correlated positively with serum ionized calcium (R ϭ 0.66; P Ͻ 0.0001). Inhibition of 11␤HSD2 activity is sufficient to significantly increase the fractional excretion of calcium and decrease serum ionized calcium, suggesting decreased tubular reabsorption of this divalent cation under conditions of renal glucocorticoid/mineralocorticoid excess. The likely site of steroid-regulated renal calcium handling appears to be the distal tubule.

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“…A lumen-negative transepithelial voltage exists across isolated cortical collecting ducts (42,43). This lumen-negative voltage is generated by the active sodium transport (42).…”

Section: Discussionmentioning

confidence: 99%

Modulation of Renal Calcium Handling by 11β-Hydroxysteroid Dehydrogenase Type 2

Ferrari

Bianchetti²,

Sansonnens³

et al. 2002

Journal of the American Society of Nephrology

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“…Recent reviews have concluded that renal Cl -transport across the mammalian CCT occurs primarily through a voltage-mediated, paracellular shunt pathway, and that a transcellular pathway across principal cells contributes little to transepithelial Cl-permeability (2-4). Regardless, Hanley et al (5) have demonstrated that microperfused rabbit CCT can reduce luminal fluid Cl-concentration to < 4 meq/liter in the presence of mineralocorticoid-stimulated Na' reabsorption. Under their experimental conditions, if passive paracellular Cl -reabsorption were the only pathway present, then the Nernst equation would predict that luminal Cl -concentration should only be reduced to 10 meq/liter.…”

mentioning

confidence: 99%

“…Elevation of intracellular cAMP increases conductive CF-reabsorption in isolated rabbit CCT (10). A variety of mechanisms might increase intracellular cAMP in CCT cells, but exposure to physiological concentrations of PGE2 stimu-lates cAMP accumulation in freshly isolated and cultured rabbit CCT (1 [1][2][3][4][5][6][7][8][9][10][11][12][13][14][15].…”

mentioning

confidence: 99%

Prostaglandin E2 activates clusters of apical Cl- channels in principal cells via a cyclic adenosine monophosphate-dependent pathway.

Ling¹,

Kokko²,

Eaton³

1994

J. Clin. Invest.

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IntroductionWe examined cell-attached patches on principal cells of primary cultured, rabbit cortical collecting tubules. Under basal conditions, apical 9-pS Cl --selective channels were observed in 9% of patches (11 / With its low baseline frequency and Ere, near resting membrane potential, this channel would not contribute significantly to transcellular Cl-flux under basal conditions. (e) However, cAMP-producing agonists (i.e., PGE2, arginine vasopressin) would increase apical C1-transport with the direction determined by the apical membrane potential. (J. Clin. Invest. 1994. 93:829-837.)

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“…Cortical collecting tubules from rabbits treated with DOCA actively reabsorb C1-from urine to blood [10,11,33]. Schuster and coworkers Ireviewed in 31] have provided strong evidence indicating that intercalated cells are at least partially responsible for transepithelial anion movements in CCT from control rabbits.…”

Section: Mechanisms Of Ouabain Swellingmentioning

confidence: 94%

Ouabain-induced cell swelling in rabbit cortical collecting tubule: NaCl transport by principal cells

Strange

1989

J. Membrain Biol.

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Ouabain had no effect on the volume of intercalated cells of DOCA-stimulated rabbit cortical collecting tubules, but caused principal cells to swell rapidly at an initial rate of 67%/min. Principal cells swelled 133% then activated regulatory volume decrease mechanisms and shrank at an initial rate of -3%/min to a new volume 13% above control. The initial rate of ouabain swelling was completely inhibited by perfusate Na+ removal or reduced 95% by luminal addition of 10(-5) M amiloride. Luminal, peritubular, or bilateral Cl- removal each caused cell shrinkages of 10% and reduced the rate of ouabain swelling by 70, 85, and 99%, respectively. The presence of an apical Cl- transport step in principal cells was confirmed by increasing luminal K+ from 5 to 53 mM, which caused cell swelling of 22%. This volume increase was completely blocked by luminal Cl- removal, but was unaffected by peritubular Cl- substitution. Perfusion of CCT with 0.1 mM acetazolomide, 0.1 mM DPC or 0.5 mM SITS caused principal cell shrinkages of 7-9% and reduced the rate of ouabain swelling by 60, 70, and 40%, respectively. The initial rate of ouabain swelling was inhibited 70% by bilateral CO2/HCO3 removal and 50% by whole animal acid loading. Taken together these results demonstrate that ouabain swelling is due to cellular NaCl accumulation and that Na+ enters the cell primarily through apical Na+ channels. Cellular Cl- entry occurs at least partially through the apical membrane and may be mediated by a Cl-/HCO3- exchanger. Brief (45-90 sec) exposure of principal cells to ouabain is associated with a rapid inhibition of Na+ and/or Cl- entry steps, whereas long-term (greater than 5 min) ouabain exposure completely blocks one or both of these transport pathways.

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Electrophysiologic study of the cortical collecting tubule of the rabbit

Cited by 26 publications

References 25 publications

Modulation of Renal Calcium Handling by 11β-Hydroxysteroid Dehydrogenase Type 2

Modulation of Renal Calcium Handling by 11β-Hydroxysteroid Dehydrogenase Type 2

Prostaglandin E2 activates clusters of apical Cl- channels in principal cells via a cyclic adenosine monophosphate-dependent pathway.

Ouabain-induced cell swelling in rabbit cortical collecting tubule: NaCl transport by principal cells

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