Vasopressin stimulates Cl- transport in ascending thin limb of Henle's loop in hamster.

Takahashi, Nobuyuki; Kondo, Yoshiaki; Itoh, Osamu; Igarashi, Yutaka; Omata, Ken; Abe, Keishi

doi:10.1172/jci117836

Cited by 26 publications

(12 citation statements)

References 21 publications

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“…The regulation of both CFTR and ClC-2 expression by AVP, the main hormone involved in the regulation of body fluid osmolality, suggests that these two proteins may be involved in the kidney's ability to concentrate and dilute the urine. This hypothesis is supported by results obtained by other authors, showing that AVP increases Cl -reabsorption in thick ascending limb of Henle's loop and cortical collecting duct cells [8,9,10,23,34,36].…”

Section: Discussionsupporting

confidence: 87%

Arginine vasopressin regulates CFTR and ClC-2 mRNA expression in rat kidney cortex and medulla

Morales

Nascimento

Capella

et al. 2001

Pflügers Arch - Eur J Physiol

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The presence of both CFTR and ClC-2 proteins in the kidney suggest that they are involved in chloride transport along the nephron but their physiological roles in this organ are not known. To further understand the role of these chloride channels we studied Wistar rats subjected to dehydration for 2 days and also the homozygous Brattleboro rats, a strain of Long-Evans rats carrying an autosomal recessive mutation that leads to a deficiency of arginine-vasopressin (AVP) secretion in the plasma. The expression of CFTR was increased in the medulla of dehydrated Wistar rats and no variation was observed in the cortex. The expression of both ClC-2 and CFTR mRNAs was low in the renal cortex and medulla of the homozygous Brattleboro rats but returned to normal levels after AVP reposition. By the use of Madine-Darby canine kidney (MDCK) type I epithelial cells, it was observed that AVP (10(-8), 10(-7) and 10(-6) M) increased CFTR mRNA expression "in vitro" but no effect was observed when changes in the medium tonicity were caused by the addition of sucrose, NaCl, manitol or urea. The modulation of both CFTR and ClC-2 mRNA by AVP, the main hormone involved in the regulation of body fluid osmolality, suggests the participation of these two chloride channels in the renal tubule transcellular chloride transport modulated by AVP.

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Section: Discussionsupporting

confidence: 87%

Arginine vasopressin regulates CFTR and ClC-2 mRNA expression in rat kidney cortex and medulla

Morales

Nascimento

Capella

et al. 2001

Pflügers Arch - Eur J Physiol

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“…One such piece of evidence is the functional regulation of chloride transport in the tAL by vasopressin. Takahashi et al [17]reported an increase in chloride permeability in the tAL induced by vasopressin treatment. They concluded that this effect was mediated by the signal through the V2 receptor, suggesting that, when vasopressin secretion is increased, i.e., under a condition where the body needs a higher urine concentration, the chloride transport in the tAL should also increase, probably through CLC-K1.…”

Section: Indirect Evidence That Clc-k1 May Be Important For Urinary Cmentioning

confidence: 99%

Severely Impaired Urine-Concentrating Ability in Mice Lacking the CLC-K1 Chloride Channel

Uchida

Marumo²

2000

Nephron Exp Nephrol

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To analyze the physiological functions of CLC-K1 in vivo, we generated mice lacking CLC-K1 by targeted gene disruption. Homozygous mutant Clcnk1–/– mice produced ∼5 times more urine than Clcnk1+/– and Clcnk1+/+ mice. After 24-hour water deprivation, Clcnk1–/– mice became severely dehydrated and lethargic. Intraperitoneal injection of the V2 agonist, deamino-Cys¹, D-Arg⁸ vasopressin, induced an increase in urine osmolarity in Clcnk1+/– and Clcnk1+/+ mice from ∼1,000 to ∼3,000 mosm/kg H₂O, whereas the increase in Clcnk1–/– mice was only from ∼600 to ∼840 mosm/kg H₂O, indicating nephrogenic diabetes insipidus in Clcnk1–/– mice. These results clearly established that CLC-K1 plays a major role in the urinary-concentrating mechanisms.

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“…Previously, we have demonstrated 3 independent factors: pH, Ca 2+, and vasopressin, that affect C1-transport. 24,25,42,55,56 In 1987, we first described how the ambient acidification of the ascending thin limb suppresses the C1-transport in hamster ascending thin limb. 24 Both luminal and basolateral acidification remarkably inhibited C1-transport.…”

Section: Regulation Of Chlorine Ion Transportmentioning

confidence: 99%

“…42 The effect of arginine vasopressin on CI-transport was investigated by measuring t r a n s e p i t h e l i a l voltage and t r a n s m u r a l 22Na-36C1 flux. In the presence ofa transmural NaC1 concentration gradient (100 mmol/L higher in the lumen), transepithelial voltage was 8.4 mV.…”

Section: Regulation Of Chlorine Ion Transportmentioning

confidence: 99%

Mechanism of sodium chloride reabsorption in the ascending thin limb of Henle's loop

Kondo

1997

Clin Exper Neph

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Vasopressin stimulates Cl- transport in ascending thin limb of Henle's loop in hamster.

Abstract: IntroductionThe effect of arginine vasopressin (AVP) on Invest. 1995Invest. . 95:1623Invest. -1627

Cited by 26 publications

References 21 publications

Arginine vasopressin regulates CFTR and ClC-2 mRNA expression in rat kidney cortex and medulla

Arginine vasopressin regulates CFTR and ClC-2 mRNA expression in rat kidney cortex and medulla

Severely Impaired Urine-Concentrating Ability in Mice Lacking the CLC-K1 Chloride Channel

Mechanism of sodium chloride reabsorption in the ascending thin limb of Henle's loop

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