Intercalated cells of the rat inner medullary collecting duct

Clapp, William L.; Madsen, Kirsten; Verlander, Jill W.; Tisher, C. Craig

doi:10.1038/ki.1987.111

Cited by 86 publications

(118 citation statements)

References 20 publications

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“…Neither aldosterone nor glucocorticoids alter UT-A1 protein abundance in the inner medullary base of adrenalectomized rats ((6) and the present study). The terminal IMCD, located in the inner medullary tip, contains a unique cell type, the IMCD cell, which is not present in other portions of the collecting duct (14,15). This suggests that the IMCD may be unique in its response to adrenal steroids, at least in terms of their effect on UT-A1 protein abundance.…”

Section: Discussionmentioning

confidence: 99%

Aldosterone Decreases UT-A1 Urea Transporter Expression via the Mineralocorticoid Receptor

Gertner¹,

Klein²,

Bailey³

et al. 2004

Journal of the American Society of Nephrology

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Abstract. Adrenalectomy in rats is associated with urinary concentrating and diluting defects. This study tested the effect of adrenal steroids on the UT-A1 urea transporter because it is involved in the urine-concentrating mechanism. Rats were adrenalectomized and given normal saline for 14 d, after which they received (1) vehicle, (2) aldosterone, or (3) spironolactone plus aldosterone. Adrenalectomy alone significantly increased UT-A1 protein in the inner medullary tip after 7 d, whereas aldosterone repletion reversed the effect. Spironolactone blocked the aldosterone-induced decrease in UT-A1, indicating that aldosterone was working via the mineralocorticoid receptor. For verifying that glucocorticoids downregulate UT-A1 protein through a different receptor, three groups of adrenalectomized rats were prepared: (1) vehicle, (2) adrenalectomy plus dexamethasone, and (3) adrenalectomy plus dexamethasone and spironolactone. Dexamethasone significantly reversed UT-A1 protein abundance increase in the inner medullary tip of adrenalectomized rats. When spironolactone was given with dexamethasone, it did not affect the dexamethasone-induced decrease in UT-A1. There was no significant change in serum vasopressin level, aquaporin 2, or Na ϩ -K ϩ -2Cl Ϫ co-transporter NKCC2/BSC1 protein abundances or UT-A1 mRNA abundance in any of the groups. In conclusion, either mineralocorticoids or glucocorticoids can downregulate UT-A1 protein. The decrease in UT-A1 does not require both steroid hormones, and each works through a different receptor.Adrenalectomy reduces urine-concentrating ability (1-3) but also inhibits acute water diuresis (4). Both glucocorticoids and mineralocorticoids must be administered to reverse the inhibition of acute water diuresis (4). Valtin and colleagues (4) showed that giving aldosterone to adrenalectomized rats after an acute water load corrected their diluting ability, whereas prednisolone corrected urine flow. These findings suggest that both adrenal steroids are involved in the regulation of urinary concentration and dilution.Urea plays an important role in the urine-concentrating mechanism (reviewed in (5)). We previously studied the effect of glucocorticoids (dexamethasone) on UT-A1 protein abundance in adrenalectomized rats. We showed that glucocorticoids decrease the protein abundance of the UT-A1 urea transporter in the inner medullary tip of adrenalectomized rats (6) and in conditions associated with excess glucocorticoid, such as uncontrolled diabetes (7,8). Presumably, in catabolic states in which glucocorticoid levels are increased, UT-A1 is downregulated to permit more nitrogenous waste to be excreted into the urine and to prevent excessive reabsorption of urea across the terminal inner medullary collecting duct (IMCD).The effect of mineralocorticoids (aldosterone) on UT-A1 protein abundance in adrenalectomized rats has not been studied. Ohara et al. (9) studied mineralocorticoid deficiency, induced by adrenalectomy with glucocorticoid replacement, and showed that it had no effect on ...

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Section: Discussionmentioning

confidence: 99%

Aldosterone Decreases UT-A1 Urea Transporter Expression via the Mineralocorticoid Receptor

Gertner¹,

Klein²,

Bailey³

et al. 2004

Journal of the American Society of Nephrology

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“…Similar to other species, the ICs of the inner medulla are lost while the abundance of ICs in the cortex increases dramatically. 14,[22][23][24][25] Surprisingly, a large proportion of these newly acquired cortical ICs appear exhibit an undifferentiated or immature phenotype, suggesting that even at one year after birth the renal CD system continues to undergo significant remodeling.…”

Section: Discussionmentioning

confidence: 99%

“…20,21 In the immediate postnatal period, the IC distribution shifts from the inner medullary CD to the cortical CD, similar to the adult distribution across several species. 14,[22][23][24][25] The full extent of the effects of obstruction on CD epithelial remodeling and on postnatal CD physiology is unknown. The purpose of the current study was to define the normal ontogeny of human IC development, and to characterize the changes in IC abundance and distribution after fetal urinary tract obstruction.…”

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confidence: 99%

Remodeling of the Fetal Collecting Duct Epithelium

Hiatt

Ivanova

Torán

et al. 2010

The American Journal of Pathology

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Congenital urinary tract obstruction induces changes to the renal collecting duct epithelium, including alteration and depletion of intercalated cells. To study the effects of obstruction on the ontogeny of intercalated cell development, we examined normal and obstructed human fetal and postnatal kidneys. In the normal human fetal kidney, intercalated cells originated in the medullary collecting duct at 8 weeks gestation and remained most abundant in the inner medulla throughout gestation. In the cortex, intercalated cells were rare at 18 and 26 weeks gestation and observed at low abundance at 36 weeks gestation. Although early intercalated cells exhibit an immature phenotype, Type A intercalated cells predominated in the inner and outer medullae at 26 and 36 weeks gestation with other intercalated cell subtypes observed rarely. Postnatally, the collecting duct epithelium underwent a remodeling whereby intercalated cells become abundant in the cortex yet absent from the inner medulla. In 18-week obstructed kidneys with mild to moderate injury, the intercalated cells became more abundant and differentiated than the equivalent age-matched normal kidney. In contrast, more severely injured ducts of the late obstructed kidney exhibited a significant reduction in intercalated cells. These studies characterize the normal ontogeny of human intercalated cell development and suggest that obstruction induces premature remodeling and differentiation of the fetal collecting duct epithelium.

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“…The rats were kept in filter-top cages with autoclaved bedding and received free access to water and a normal protein diet (NIH-31; Ziegler Brothers, Gardner, PA) unless otherwise indicated below. The kidneys were placed into chilled (17 Њ C), isotonic, dissecting solution to isolate initial (IMCD 1 ) or terminal (IMCD 2 or IMCD 3 ) IMCD subsegments (18,19) as described (12,20).…”

Section: Tissue Preparationmentioning

confidence: 99%

Active sodium-urea counter-transport is inducible in the basolateral membrane of rat renal initial inner medullary collecting ducts.

Kato¹,

Sands²

1998

J. Clin. Invest.

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Rat inner medullary collecting ducts (IMCD 3 s) possess a luminal Na ϩ -dependent, active urea secretory transport process, which is upregulated by water diuresis. In this study of perfused IMCDs microdissected from base (IMCD 1 ), middle (IMCD 2 ), or tip (IMCD 3 ) of the inner medulla, we tested whether furosemide diuresis alters active urea transport. Rats received furosemide (10 mg/d s.c. for 3-4 d) and were compared with pair-fed control rats. Furosemide significantly decreased urine osmolality and urea clearance, and increased blood urea nitrogen. IMCD 3 s from furosemidetreated rats had significantly lower rates of active urea secretion than IMCD 3 s from control rats. IMCD 2 s showed no active urea transport in control or furosemide-treated rats.

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Intercalated cells of the rat inner medullary collecting duct

Cited by 86 publications

References 20 publications

Aldosterone Decreases UT-A1 Urea Transporter Expression via the Mineralocorticoid Receptor

Aldosterone Decreases UT-A1 Urea Transporter Expression via the Mineralocorticoid Receptor

Remodeling of the Fetal Collecting Duct Epithelium

Active sodium-urea counter-transport is inducible in the basolateral membrane of rat renal initial inner medullary collecting ducts.

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