Reverse pharmacological effect of loop diuretics and altered rBSC1 expression in rats with lithium nephropathy

Michimata, Mari; Fujita, Sayuri; Araki, Tsutomu; Mizukami, Kazuhiko; Kazama, Itsuro; Muramatsu, Yukiko; Suzuki, Michiko; Kimura, Tokihisa; Sasaki, Sei; Imai, Yutaka; Matsubara, Mitsunobu

doi:10.1046/j.1523-1755.2003.00738.x

Cited by 13 publications

(5 citation statements)

References 23 publications

(13 reference statements)

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“…Immunoblotting with a specific antibody against AQP2 was performed as previously described [20]. Briefly, the renal inner medulla was homogenized in 2 ml of PBS, 1% Triton, 1% deoxycholate, 0.1% SDS, and 0.1 m M phenylmethylsulfonyl fluoride.…”

Section: Methodsmentioning

confidence: 99%

Residual Urinary Concentrating Ability and AQP2 Expression in a Rat Model for Chronic Renal Failure

Suzuki

Hatano²,

Michimata³

et al. 2004

Nephron Physiol

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Background: In chronic renal failure (CRF), a defect in urinary concentrating ability develops gradually as the renal failure progresses. Although several molecular mechanisms associated with renal urinary concentration are reported to be impaired in a rat model for renal failure, the mechanisms underlying residual urinary concentration ability in CRF remain to be elucidated. Methods: Rats that underwent an 8-week recovery period after 5/6 nephrectomy were used as the model for CRF. Urinary concentration was induced by 24-hour water restriction. Plasma osmolality and arginine vasopressin (AVP) were measured from blood sampled by inserting a catheter into the femoral artery before and after the water restriction. AQP2 mRNA expression in the inner medulla was examined by competitive PCR and in situ hybridization, and protein expression, by Western blotting. Rats that underwent sham operation were used as control. Results: Water restriction significantly reduced urine volume and increased urine osmolality in CRF rats, although such changes were much less than those in sham-operated rats. Plasma AVP was elevated at the basal condition, and further elevation was noted after water restriction. AQP2 mRNA signals were significantly intensified by water restriction even in CRF rats, although the increase was limited as in the case of urine osmolality. Western blotting also showed a small but significant enhancement of protein signals in response to water restriction in CRF rats. Conclusions: We noted a weak but significant response of AQP2 expression to dehydration in CRF rats. This response in the collecting duct may be one of the factors contributing to residual urinary concentrating ability in CRF.

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Section: Methodsmentioning

confidence: 99%

Residual Urinary Concentrating Ability and AQP2 Expression in a Rat Model for Chronic Renal Failure

Suzuki

Hatano²,

Michimata³

et al. 2004

Nephron Physiol

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“…Immunoblotting using a specific antibody against AQP2 or rBSC1 was performed as previously described [17,30,31]. Briefly, after dividing the harvested kidneys into three parts-cortex, outer medulla, and inner medulla-the renal outer medulla and the inner medulla were separately homogenized in 2 mL of phosphatebuffered saline (PBS), 1% Triton, 1% deoxycholate, 0.1% sodium dodecyl sulfate (SDS), and 0.1 mmol/L phenylmethylsulfonyl fluoride (PMSF) for protein extraction.…”

Section: Immunoblottingmentioning

confidence: 99%

“…Electrolyte and urea concentrations in the renal medulla were determined according to previous studies in which solute accumulation in the renal medulla was measured [17,30]. Briefly, the renal inner medulla was separated, put inside a microcentrifuge tube, and quickly weighed.…”

Section: Measurements Of Electrolytes and Urea In Renal Medullamentioning

confidence: 99%

BSC1 inhibition complements effects of vasopressin V2 receptor antagonist on hyponatremia in SIADH rats

Kazama

Hatano

Michimata

et al. 2005

Kidney International

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“…The diuretics acetazolamide (50-52), amiloride (12)(13)(14)(46)(47)(48)(49), furosemide (61), and hydrochlorothiazide (41-45) have been found to paradoxically reduce urine output in Li-NDI. While all of these interventions have been documented to reduce polyuria/polydipsia, the underlying mechanisms remain unclear.…”

Section: Discussionmentioning

confidence: 99%

Nrf2 activation protects against lithium-induced nephrogenic diabetes insipidus

Jobbagy¹,

Vitturi²,

Salvatore³

et al. 2020

JCI Insight

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Reverse pharmacological effect of loop diuretics and altered rBSC1 expression in rats with lithium nephropathy

Abstract: Our results suggest that dehydration or high plasma AVP results in an enhanced rBSC1 expression in Li nephropathy, and that rBSC1 expression is closely associated with the adverse effects of Li ions on collecting duct function.

Cited by 13 publications

References 23 publications

Residual Urinary Concentrating Ability and AQP2 Expression in a Rat Model for Chronic Renal Failure

Residual Urinary Concentrating Ability and AQP2 Expression in a Rat Model for Chronic Renal Failure

BSC1 inhibition complements effects of vasopressin V2 receptor antagonist on hyponatremia in SIADH rats

Nrf2 activation protects against lithium-induced nephrogenic diabetes insipidus

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