Luminal chloride modulates rat distal tubule bidirectional bicarbonate flux in vivo.

Levine, David Z.; Vandorpe, David H.; Iacovitti, Michelle

doi:10.1172/jci114637

Cited by 27 publications

(12 citation statements)

References 21 publications

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“…Our findings that bicarbonate secretion may modulate the apparent rate of net bicarbonate absorption support the view of Levine et al, who have assigned an important role to bidirectional bicarbonate transport in the distal tubule (31).…”

Section: Methodssupporting

confidence: 92%

See 1 more Smart Citation

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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Section: Methodssupporting

confidence: 92%

“…Bicarbonate absorption is enhanced by acidosis and reduced by metabolic alkalosis (7). Bicarbonate absorption is also stimulated by low tubule perfusion rates ( 10), by fasting( 11), high aldosterone (Kunau, R., personal communication) and vasopressin levels (3), and by low luminal chloride (31 ).…”

Section: Methodsmentioning

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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“…9,13 In the distal convoluted tubule, alkalosis can induce HCO 3 secretion, which is inhibited by the removal of luminal chloride; it is likely that such effects emanate from the connecting tubule. 14 In perfused cortical collecting ducts, HCO 3 2 is secreted in tubules from CDA rats and is dependent on luminal chloride, whereas it is reabsorbed in normal rats. 15 The magnitude and direction of HCO 3 2 transport is dependent upon the degree of alkalosis and chloride repletion in vivo at the time of tubule harvesting.…”

mentioning

confidence: 99%

It Is Chloride Depletion Alkalosis, Not Contraction Alkalosis

Luke

Galla

2012

Journal of the American Society of Nephrology

104

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Maintenance of metabolic alkalosis generated by chloride depletion is often attributed to volume contraction. In balance and clearance studies in rats and humans, we showed that chloride repletion in the face of persisting alkali loading, volume contraction, and potassium and sodium depletion completely corrects alkalosis by a renal mechanism. Nephron segment studies strongly suggest the corrective response is orchestrated in the collecting duct, which has several transporters integral to acid-base regulation, the most important of which is pendrin, a luminal Cl/HCO 3 2 exchanger. Chloride depletion alkalosis should replace the notion of contraction alkalosis.

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“…We have recently reported that net bicarbonate secretion' can occur in rat distal tubules in vivo and this response is modulated by changes in luminal chloride concentration (1). Because we found B-type intercalated cells in rat surface distal Portions of this work have appeared in abstract form (1990.…”

Section: Introductionmentioning

confidence: 92%

“…1. Throughout this paper, unless otherwise stated, the term "secretion of bicarbonate" refers to absolute net bicarbonate accumulation in the tubular lumen which is determined by the sum of opposing unidirectional secretory and reabsorptive fluxes.…”

Section: Introductionmentioning

confidence: 99%

Bicarbonate secretion in vivo by rat distal tubules during alkalosis induced by dietary chloride restriction and alkali loading.

Levine¹,

Iacovitti²,

Harrison³

1991

J. Clin. Invest.

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Luminal chloride modulates rat distal tubule bidirectional bicarbonate flux in vivo.

Cited by 27 publications

References 21 publications

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

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

It Is Chloride Depletion Alkalosis, Not Contraction Alkalosis

Bicarbonate secretion in vivo by rat distal tubules during alkalosis induced by dietary chloride restriction and alkali loading.

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