Decreased Expression of Aquaporin Water Channels in Denervated Rat Kidney

Lee, Jong-Un; Yoo, Kwangjay; Kim, Soo Wan; Jung, Kwang‐Woo; Kwon, Seong; Lee, Yeon Kyung; Kim, Wan-Young; Kim, Jin; Choi, Ki Chul

doi:10.1159/000092918

Cited by 18 publications

(13 citation statements)

References 27 publications

(12 reference statements)

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“…However, Liu et al[ 45] reported no changes in plasma levels of AVP in animals chronically treated with L -NAME in the same dose used in this study; while Zanchi et al[ 46] and Sander et al [47] reported increased activity of the sympathetic nervous system in this model of hypertension, which, according to Lee et al[ 48], should cause upregulation of AQP2 expression.…”

Section: Discussionmentioning

confidence: 53%

Renal Sodium-Glucose Cotransporter Activity and Aquaporin-2 Expression in Rat Kidney during Chronic Nitric Oxide Synthase Inhibition

et al. 2007

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Background/Aims: The renal sodium glucose cotransporter (SGLT2) and the water channel aquaporin-2 (AQP2) play a critical role in tubular sodium and water reabsorption and in the regulation of extracellular fluid volume both in physiologic and pathophysiologic conditions. However, there is little information about SGLT2 and AQP2 expression and/or activity in hypertension and there are no reports during hypertension induced by chronic nitric oxide synthase (NOS) inhibition. Methods: Hypertension was induced in rats by oral administration of N^G-nitro-L-arginine methyl ester (L-NAME) (20 mg/kg/24 h) for 6 (H6) or 12 (H12) weeks. SGLT2 activity was measured using α-¹⁴C-methylglucose active uptake. The expression level of transporters was assessed by immunohistochemistry and/or immunoblotting. Results: SGLT2 activity was reduced in both H6 and H12; this was due neither to a decrease in SGLT2 expression nor to a change in membrane phospholipid composition. In H6, AQP2 expression diminished only in the inner medulla (IM), while in H12 it diminished in both outer (OM) and IM. This reduced expression of AQP2 may partially account for the increased urinary volume and decreased urinary osmolality in H12, since we obtained a strong correlation between AQP2 expression and these urinary parameters in both OM and IM. Conclusion: We propose that in rats in which hypertension is induced by NOS inhibition, SGLT2 activity and AQP2 expression are modified to compensate for the elevated arterial pressure. However, we cannot discount the possibility that the observed changes are due to the decrease in NO production itself.

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Section: Discussionmentioning

confidence: 53%

Renal Sodium-Glucose Cotransporter Activity and Aquaporin-2 Expression in Rat Kidney during Chronic Nitric Oxide Synthase Inhibition

et al. 2007

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“…According to the results from experiments with denervated rat kidneys, a reduction in sympathetic nervous stimulation reduced AQP2 expression (23), and the authors suggest that renal sympathetic nerve activity may play an excitatory role in AQP2 regulation. Methylprednisolone treatment induced changes in systemic hemodynamics, i.e.…”

Section: Discussionmentioning

confidence: 99%

Direct effect of methylprednisolone on renal sodium and water transport via the principal cells in the kidney

Lauridsen

Vase²,

Bech³

et al. 2010

European Journal of Endocrinology

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Background: Glucocorticoids influence renal concentrating and diluting ability. We tested the hypothesis that methylprednisolone treatment increased renal water and sodium absorption by increased absorption via the aquaporin-2 (AQP2) water channels and the epithelial sodium channels (ENaCs) respectively. Methods: The effect of methylprednisolone was measured during fasting in a randomized, placebocontrolled, single-blinded cross-over study of 15 healthy humans. The subjects received a standardized diet on day 1, fasted on day 2, and received 500 mg methylprednisolone intravenously on day 3. The effect variables were urinary excretions of AQP2 (u-AQP2), urinary excretion of the b-fraction of the ENaC (u-ENaC b ), cAMP (u-cAMP), prostaglandin E 2 (u-PGE 2 ), free water clearance (C H 2 O ), and fractional excretion of sodium (FE Na ), and plasma vasopressin (p-AVP), angiotensin II (p-Ang II), aldosterone (p-Aldo), atrial natriuretic peptide (p-ANP), and brain natriuretic peptide (p-BNP). Results: Methylprednisolone treatment increased u-AQP2, u-ENaC b , and p-AVP significantly, but did not change u-cAMP, C H 2 O , and FE Na . P-ANP increased during methylprednisolone treatment, but after the increase in u-AQP2 and u-ENaC b . U-PGE 2 , p-Ang II, and p-BNP were unchanged. Heart rate increased and diastolic blood pressure fell. Conclusions: Methylprednisolone increased u-AQP2 and u-ENaC. Neither the AVP-cAMP axis nor changes in the renin-angiotensin-Aldo system, or the natriuretic peptide system seems to bear a causal relationship with the increase in either u-AQP2 or u-ENaC. Most probably, the effect is mediated via a direct effect of methylprednisolone on the principal cells. The lack of decrease in urinary output and sodium reabsorption most likely can be attributed to the diuretic and natriuretic properties of the increased secretion of ANP.

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“…It has been suggested that the potential cross-talk between the two kidneys is regulated by a number of mechanistic pathways, including the renal nerves. For example, neural regulation of aquaporin in kidneys has been found following unilateral denervation, reducing the renal norepinephrine content in the contralateral kidney [10] . These changes were mediated by reduced AQP1-4 protein expression in the obstructed kidney, while an increased abundance in the contralateral kidney was observed [10] .…”

mentioning

confidence: 99%

Regulation of Aquaporins and Sodium Transporter Proteins in the Solitary Kidney in Response to Partial Ureteral Obstruction in Neonatal Rats

Topçu¹,

Nørregaard²,

Pedersen

et al. 2011

Urol Int

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Unilateral ureteral obstruction (UUO) impairs function of the obstructed kidney, and the contralateral nonobstructed kidney compensates depending on the degree and duration of UUO. This study aimed to determine the hemodynamic and molecular changes in the solitary kidney in response to partial ureteral obstruction (PUO) where any compensation from the contralateral kidney was eliminated so that all observed changes in the kidney tissue occurred in the kidney with PUO. Newborn rats were subjected to unilateral left nephrectomy (UNX) within the first 48 h of life and a subset of UNX rats was subjected to severe PUO of the right kidney at day 14. Renal blood flow and whole kidney volume were measured with MRI at week 10. The renal protein abundance of aquaporin 1 (AQP1), AQP2 and AQP3 as well as Na,K-ATPase, NaPi-2 (type 2 sodium-phosphate cotransporter) and NHE3 (type 3 sodium-proton exchanger) were examined by immunoblotting and immunocytochemistry. At 10 weeks of age, the protein abundance of AQP2, AQP3, Na,K-ATPase, NaPi-2 and NHE3 were increased in response to PUO. In contrast, AQP1 expression was markedly decreased compared to sham-operated rats. These findings were confirmed by immunohistochemistry. GFR, urine osmolality and urine sodium excretion were reduced and kidney weight increased in response to PUO. In conclusion, the present study demonstrated major changes in the protein abundance of renal AQP1, AQP2 and AQP3 and sodium transporters in the solitary PUO kidney. These changes were paralleled by decreased urinary sodium excretion and a significant reduction in urinary osmolality from the obstructed kidney, suggesting a functional association between the molecular changes and the ability of the obstructed kidney to handle sodium and water in this solitary kidney model.

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Decreased Expression of Aquaporin Water Channels in Denervated Rat Kidney

Cited by 18 publications

References 27 publications

Renal Sodium-Glucose Cotransporter Activity and Aquaporin-2 Expression in Rat Kidney during Chronic Nitric Oxide Synthase Inhibition

Renal Sodium-Glucose Cotransporter Activity and Aquaporin-2 Expression in Rat Kidney during Chronic Nitric Oxide Synthase Inhibition

Direct effect of methylprednisolone on renal sodium and water transport via the principal cells in the kidney

Regulation of Aquaporins and Sodium Transporter Proteins in the Solitary Kidney in Response to Partial Ureteral Obstruction in Neonatal Rats

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