Acidification of luminal fluid by the rabbit cortical collecting tubule perfused in vitro

Koeppen, Bruce M.; Helman, S. I.

doi:10.1152/ajprenal.1982.242.5.f521

Cited by 47 publications

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“…VT did not significantly change with DIDS (paired A = -1.0+1.9 mV, NS). These results are consistent with the known effects of basolateral disulfonic stilbenes on acidification in the turtle bladder (13), medullary collecting tubule (14), and cortical collecting tubule (15), and demonstrate that bath DIDS was a potent inhibitor of H' secretion in our system. In time controls from acid-loaded, starved rabbits (n = 4, not shown), the HCO3 reabsorptive rate did not change (1.94±1.32 period 1, 1.45±1.63 period 2, A = NS).…”

Section: Methodssupporting

confidence: 91%

Cyclic adenosine monophosphate-stimulated bicarbonate secretion in rabbit cortical collecting tubules.

Schuster¹

1985

J. Clin. Invest.

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We studied the effects of cyclic AMP (cAMP) on HCO3 transport by rabbit cortical collecting tubules perfused in vitro. Net HCO3 secretion was observed in tubules from NaHCO3-loaded rabbits. 8-Bromo-cAMP-stimulated net HCO3-secretion, whereas secretion fell with time in control tubules. Both isoproterenol and vasopressin (ADH) are known to stimulate adenylate cyclase in this epithelium; however, only isoproterenol stimulated net HCO3 secretion.The mechanism of cAMP-stimulated HCO3 secretion was examined. If both HCO3 and H+ secretion were to occur simultaneously in tubules exhibiting net HCO3-secretion, cAMP might increase the net HCO3-secretory rate by inhibiting H+ secretion, by stimulating HCO3 secretion, or both. These possibilities were examined using basolateral addition of the disulfonic stilbene (4,4'-diisothiocyanostilbene-2,2'-disulfonate (DIDS). In acidifying tubules from NH4Cl-loaded rabbits, DIDS eliminated HCO3-reabsorption, a result consistent with known effects of DIDS as an inhibitor of H+ secretion. In contrast, cAMP left acidification (H+ secretion) intact. DIDS applied to HCO3 secretory tubules failed to increase the HCO3 secretory rate, indicating minimal H+ secretion in HCO3-secreting tubules. Thus, inhibition of H+ secretion by cAMP could not account for the cAMP-induced stimulation of net HCO3 secretion.cAMP-stimulated HCO3 secretion was reversibly eliminated by 0 Cl perfusate, whereas luminal DIDS had no effect. Bath amiloride (1 mM) failed to eliminate cAMP-stimulated HCO3 secretion when bath [Na'J was 145 mM or 5 mM. cAMP depolarized the transepithelial voltage. The collected fluid [HCO3j after cAMP could be accounted for by electrical driving forces, suggesting that cAMP stimulates passive HCO3 secretion. However, cAMP did not alter HCO3 permeability measured under conditions expected to inhibit transcellular HCO3 movement (O Cl-solutions and bath DIDS). This measured HCO3 permeability was not high enough to account, by passive diffusion, for the HCO3 fluxes observed in Cl--containing solutions.We conclude the following: 1) cAMP increased net HCO3 secretion by stimulating HCO3 secretion and not by

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Section: Methodssupporting

confidence: 91%

Cyclic adenosine monophosphate-stimulated bicarbonate secretion in rabbit cortical collecting tubules.

Schuster¹

1985

J. Clin. Invest.

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“…Sodium and potassium were measured by flame photometry. Glomerular filtration rate was (19,20), the decreased FEK is further evidence for a distal tubular dysfunction in FAS patients.…”

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confidence: 92%

“…Decreased sodium delivery to the distal nephron cannot account for the impairment in urinary gotassium excretion observed in FA$ patients. As shown in Table 4 (19,20).…”

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confidence: 98%

Impaired Renal Acidification in Infants with Fetal Alcohol Syndrome

Assadi

Ziai

1985

Pediatr Res

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ABSTRACT. Urinary acidification was studied in six unrelated infants with fetal alcohol syndrome and eight healthy age-matched infants. Creatinine clearance, fractional sodium excretion, plasma renin activity, and plasma aldosterone were normal in all patients but fractional potassium excretion was lower in the patients than in the controls (p = 0.0001). After ammonium chloride loading, minimum urine pH was significantly higher in FAS patients than in control subjects (5.5 + 0.1 and 4.7 + 0.1, respectively, p = 0.00005). Net acid excretion was also lower in the patients (24.5 2 1.7 Eq/min) than in the controls (27.8 +. While evaluating patients with the FAS it became apparent that episodes of hyperchloremic metabolic acidosis associated with alkaline urine were common during the period of dehydration. Review of the literature showed rlo report of impaired renal acid~fication associated with the syndrome (1-4). Therefore, a prospective study of renal acidification was performed in six infants with FAS to determine if there is any relationship between perinatal ethanol exposure and impaired urinary acidification in the development of metabolic acidosis.

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“…Several transport mechanisms have been implicated in this process including Na'-H+ exchange, electrogenic H+ secretion and K-H exchange (12)(13)(14)(15). In addition, bicarbonate secretion by electroneutral exchange of luminal Cl for HCO3 also affects net bicarbonate transport ( 16).…”

Section: Introductionmentioning

confidence: 99%

“…Little is known about the mechanisms ofacidification in the distal convoluted tubule, an extension of the thick ascending limb in which Na+-H+ exchange has been observed in the rat kidney ( 19). On the other hand, the initial collecting tubule contains several populations of intercalated cells, known to be responsible for both H + and HCO-secretion ( 15,16,20,21).…”

Section: Introductionmentioning

confidence: 99%

Renal bicarbonate reabsorption in the rat. IV. Bicarbonate transport mechanisms in the early and late distal tubule.

Wang¹,

Malnic²,

Giebisch³

et al. 1993

J. Clin. Invest.

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Bicarbonate transport was studied in vivo by separate microperfusion experiments of early and late distal tubules. Total CO2 was measured by microcalorimetry and fluid absorption by 3H-inulin. Significant bicarbonate absorption was observed in all experimental conditions. Bicarbonate transport was loaddependent upon increasing the luminal bicarbonate concentration from 15 to 50 mM in both early and late distal tubule segments and remained constant at higher concentrations at a maximum rate of 100-110 pmol/min per mm. At low lumen bicarbonate concentrations (15 mM), higher rates of bicarbonate absorption were observed in early (32.9±4.57 pmol/min per mm) as compared to late distal tubules (10.7±3.1 pmol/ min per mm). Amiloride and ethyl-isopropylamiloride both inhibited early but not late distal tubule bicarbonate absorption whereas acetazolamide blocked bicarbonate transport in both tubule segments. Fluid absorption was significantly reduced in both tubule segments by amiloride but only in early distal tubules by ethyl-isopropylamiloride. Substitution of lumen chloride by gluconate increased bicarbonate absorption in late but not in early distal tubules. Bafilomycin Al, an inhibitor of HATPase, inhibited late and also early distal tubule bicarbonate absorption, the latter at higher concentration. After 8 d on a low K diet, bicarbonate absorption increased significantly in both early and late distal tubules. Schering compound 28080, a potent H-K ATPase inhibitor, completely blocked this increment of bicarbonate absorption in late but not in early distal tubule. The data suggest bicarbonate absorption via Na+-H+ exchange and H-ATPase in early, but only by amiloride-insensitive H' secretion (H-ATPase) in late distal tubules. The study also provides evidence for activation of K+-H+ exchange in late distal tubules of K depleted rats. Indirect evidence implies a component of chloride-dependent bicarbonate secretion in late distal tubules and suggests that net bicarbonate transport at this site results from bidirectional bicarbonate movement. (J. Clin.

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Acidification of luminal fluid by the rabbit cortical collecting tubule perfused in vitro

Cited by 47 publications

References 0 publications

Cyclic adenosine monophosphate-stimulated bicarbonate secretion in rabbit cortical collecting tubules.

Cyclic adenosine monophosphate-stimulated bicarbonate secretion in rabbit cortical collecting tubules.

Impaired Renal Acidification in Infants with Fetal Alcohol Syndrome

Renal bicarbonate reabsorption in the rat. IV. Bicarbonate transport mechanisms in the early and late distal tubule.

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