Amelioration of polyuria in nephrogenic diabetes insipidus due to aquaporin‐2 deficiency

Hochberg, Zèev; Even, Lea; Danon, Abraham

doi:10.1046/j.1365-2265.1998.00426.x

Cited by 24 publications

(20 citation statements)

References 21 publications

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“…In nephrogenic diabetes insipidus, COX inhibitors are often used in combination with hydrochlorothiazide to ameliorate polyuria (50). The beneficial effect of COX inhibitors is seen in patients with mutations in the arginine-vasopressin receptor 2 gene as well as in the aquaporin-2 water channel gene (51). Whether under this clinical situation EP1, EP3, and/or EP4 receptors are involved needs to be clarified, but we suggest that the same PGE 2 -mediated mechanism may be operable in these patients.…”

Section: Discussionmentioning

confidence: 99%

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

Nüsing

Treude

Weißenberger

et al. 2005

Journal of the American Society of Nephrology

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Increased formation of prostaglandin E 2 (PGE 2 ) is a key part of hyperprostaglandin E syndrome/antenatal Bartter syndrome (HPS/aBS), a renal disease characterized by NaCl wasting, water loss, and hyperreninism. Inhibition of PGE 2 formation by cyclo-oxygenase inhibitors significantly lowers patient mortality and morbidity. However, the pathogenic role of PGE 2 in HPS/aBS awaits clarification. Chronic blockade of the Na-K-2Cl co-transporter NKCC2 by diuretics causes symptoms similar to HPS/aBS and provides a useful animal model. In wild-type (WT) mice and in mice lacking distinct PGE 2 receptors (EP1 In summary, these findings demonstrate that the EP4 receptor mediates PGE 2 -induced renin secretion and that EP1, EP3, and EP4 receptors all contribute to enhanced PGE 2 -mediated salt and water excretion in the HPS/aBS model.

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Section: Discussionmentioning

confidence: 99%

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

Nüsing

Treude

Weißenberger

et al. 2005

Journal of the American Society of Nephrology

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“…However, not all patients respond well to diuretic therapy, and those who respond only partially may be the 10% of patients with mutations in their AQP2 gene and not the 90% with mutations in their V2R gene (49). Since diuretic therapy also induces a mild state of dehydration, it is possible that the dehydration increases water reabsorption in patients with normal AQP2 by an increase in NOS.…”

Section: Figure 12mentioning

confidence: 99%

Nitric oxide and atrial natriuretic factor stimulate cGMP-dependent membrane insertion of aquaporin 2 in renal epithelial cells

Bouley¹,

Breton²,

Sun³

et al. 2000

J. Clin. Invest.

210

218

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“…The importance of PGE 2 in the regulation of water metabolism is further signified by the association between altered urinary PGE 2 excretion and conditions of perturbed urinary concentrating ability (18,30,41). In nephrogenic diabetes insipidus (NDI) caused either by mutation in the AVPR2 or AQP2 genes, hypercalcemia, or lithium treatment, there is a peripheral resistance to ADH (24,29).…”

mentioning

confidence: 99%

“…In nephrogenic diabetes insipidus (NDI) caused either by mutation in the AVPR2 or AQP2 genes, hypercalcemia, or lithium treatment, there is a peripheral resistance to ADH (24,29). Patients suffer from severe polyuria and hyposmolar urine in the presence of normal or high plasma levels of ADH, whereas urinary PGE 2 excretion is increased (18,30,41,47). These observations have led to the use of COX inhibitors to decrease urine volume in NDI patients (18,26,37,45).…”

mentioning

confidence: 99%

“…Patients suffer from severe polyuria and hyposmolar urine in the presence of normal or high plasma levels of ADH, whereas urinary PGE 2 excretion is increased (18,30,41,47). These observations have led to the use of COX inhibitors to decrease urine volume in NDI patients (18,26,37,45). Moreover, patients with central diabetes insipidus (CDI), which is caused by the lack of ADH secretion, also suffer from polyuria and hyposmolar urine (27).…”

mentioning

confidence: 99%

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Altered expression of COX-1, COX-2, and mPGES in rats with nephrogenic and central diabetes insipidus

Kotnik¹,

Nielsen²,

Kwon³

et al. 2005

American Journal of Physiology-Renal Physiology

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Kotnik, Primož, Jakob Nielsen, Tae-Hwan Kwon, Ciril Kržiš-nik, Jørgen Frøkiaer, and Søren Nielsen. Altered expression of COX-1, COX-2, and mPGES in rats with nephrogenic and central diabetes insipidus. Am J Physiol Renal Physiol 288: F1053-F1068, 2005. First published January 11, 2005 doi:10.1152/ajprenal.00114.2004Prostaglandins have an important role in renal salt and water reabsorption. PGE 2 is the main kidney prostaglandin and is thought to be mainly produced in the kidney inner medulla (IM). There are indications that PGE2 synthesis in nephrogenic (NDI) and central (CDI) diabetes insipidus is altered. We hypothesize that the expression of the major PGE 2 synthesis enzymes cyclooxygenases 1 and 2 (COX-1, COX-2) and membrane-associated PGE2 synthase (mPGES) is altered in the kidneys of rats with NDI and CDI. Wistar rats treated with lithium for 4 wk were used as the NDI model. One-half of the NDI model rats were additionally dehydrated for 48 h. Brattleboro (BB) rats that lack endogenous antidiuretic hormone were used as the CDI model. Expression and localization of COX-1, COX-2, and mPGES in IM, inner stripe of outer medulla (ISOM), and cortex were determined by immunoblotting and immunohistochemistry. In lithium-induced NDI, expression of COX-1, COX-2, and mPGES was markedly decreased in IM. In ISOM and cortex, COX-1 expression was marginally reduced and mPGES expression was unaltered. COX-2 expression was undetected in ISOM and marginally increased in cortex. Consistent with this, the density of COX-2-expressing cells in macula densa was significantly increased, indicating differential regulation of COX-2 in IM and cortex. Dehydration of NDI rats resulted in a marked increase in COX-2 immunolabeling in IM interstitial cells, and there was no significant change in COX-1 and mPGES expression in any kidney zone. Treatment of DDAVP in BB rats for 6 days resulted in a markedly increased expression of COX-1, COX-2, and mPGES in IM. In the cortex, there were no changes in the expression of COX-1 and mPGES, whereas COX-2 expression was decreased. These results identify markedly reduced expression of COX-1, COX-2, and mPGES in IM in lithium-induced NDI. Furthermore, there were major changes in the expression of COX-1, COX-2, and mPGES in rats with CDI.cyclooxygenase-2; DDAVP; inner medullary interstitial cell; medullary osmolality; membrane-associated prostaglandin E 2 synthase; prostaglandin; urine concentration PROSTAGLANDINS, WHICH FUNCTION as autocrine and paracrine lipid mediators, play important roles in a variety of regulatory homeostatic mechanisms (36). In the kidney, prostaglandins have an important role in affecting renal hemodynamics, renin release, tubular sodium, and water reabsorption (12). The main prostaglandin in the kidney is prostaglandin E 2 (PGE 2 ), which is synthesized from arachidonic acid in a two-step enzymatic reaction. Arachidonic acid is first converted to an unstable intermediate PGH 2 by one of the two cyclooxygenase isoforms, COX-1 or COX-2. This rate-limiting step is then followe...

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Amelioration of polyuria in nephrogenic diabetes insipidus due to aquaporin‐2 deficiency

Cited by 24 publications

References 21 publications

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

Dominant Role of Prostaglandin E2 EP4 Receptor in Furosemide-Induced Salt-Losing Tubulopathy

Nitric oxide and atrial natriuretic factor stimulate cGMP-dependent membrane insertion of aquaporin 2 in renal epithelial cells

Altered expression of COX-1, COX-2, and mPGES in rats with nephrogenic and central diabetes insipidus

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