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      Decreased Expression of Aquaporin Water Channels in Denervated Rat Kidney

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          Aims: A neural mechanism regulating aquaporin (AQP) water channels in the kidney was investigated. Methods: Male Sprague-Dawley rats were used. Renal denervation was induced by painting the renal vessels with 10% phenol. The expression of AQP1–4 proteins was determined in the denervated and contralateral kidneys. The expression was also examined in rats which were renally denervated and subjected to water restriction or deoxycorticosterone acetate (DOCA)-salt treatment. Results: Following the unilateral denervation, tissue contents of norepinephrine were significantly decreased in the denervated kidney, while increased in the contralateral kidney. Accordingly, the expression of AQP1–4 proteins was decreased by 15–40% in the denervated kidney, and increased by 30–50% in the contralateral kidney. Immunohistochemistry of AQP2 confirmed its decreases in the denervated kidney and increases in the contralateral kidney. In bilaterally denervated rats, the urine flow increased along with decreased osmolarity. The water restriction increased the expression of AQP channels, however, the magnitude of which was lower in the denervated than in the contralateral kidney. Renal denervation decreased the degree of DOCA-salt hypertension, along with lower expression of AQP channels. Conclusion: It is suggested that the sympathetic nerve should play a specific excitatory role in the regulation of AQP channels in the kidney.

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          COX-2 inhibition prevents downregulation of key renal water and sodium transport proteins in response to bilateral ureteral obstruction.

          Bilateral ureteral obstruction (BUO) is associated with marked changes in the expression of renal aquaporins (AQPs) and sodium transport proteins. To examine the role of prostaglandin in this response, we investigated whether 24-h BUO changed the expression of cyclooxygenases (COX-1 and -2) in the kidney and tested the effect of the selective COX-2 inhibitor parecoxib (5 via osmotic minipumps) on AQPs and sodium transport. Sham and BUO kidneys were analyzed by semiquantitative immunoblotting, and a subset of kidneys was perfusion fixed for immunocytochemistry. BUO caused a significant 14-fold induction of inner medullary COX-2 (14.40 +/- 1.8 vs. 1.0 +/- 0.4, n = 6; P < 0.0001) and a reduction in medullary tissue osmolality, whereas COX-1 did not change. Immunohistochemistry confirmed increased COX-2 labeling associated with medullary interstitial cells. COX isoforms did not change in cortex/outer medulla after 24-h BUO. In BUO kidneys, inner medullary AQP2 expression was reduced, and this decrease was prevented by parecoxib. In the inner stripe of outer medulla, the type 3 Na(+)/H(+) exchanger (NHE3) and apical Na(+)-K(+)-2Cl(-) cotransporter (BSC-1) were significantly reduced by BUO, and this decrease was significantly attenuated by parecoxib. Immunohistochemistry for AQP2, NHE3, and BSC-1 confirmed the effect of parecoxib. Parecoxib had no significant effect on the Na-K-ATPase alpha(1)-subunit, type II Na-P(i) cotransporter, or AQP3. In conclusion, acute BUO leads to marked upregulation of COX-2 in inner medulla and selective COX-2 inhibition prevents dysregulation of AQP2, BSC-1, and NHE3 in response to BUO. These data indicate that COX-2 may be an important factor contributing to the impaired renal water and sodium handling in response to BUO.
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            Upregulation of aquaporin-2 water channel expression in chronic heart failure rat.

            Aquaporin-2 (AQP2) mediates vasopressin-regulated collecting duct water permeability. Chronic heart failure (CHF) is characterized by abnormal renal water retention. We hypothetized that upregulation of aquaporin-2 water channel could account for the water retention in CHF. Male rats underwent either a left coronary artery ligation, a model of CHF, or were sham operated. 31-33 d after surgery, mean arterial pressure (MAP) and cardiac output were measured in conscious animals, and the animals were killed 24 h later. Cardiac output (CO) and plasma osmolality were significantly decreased and plasma vasopressin increased in the CHF as compared to the sham-operated rats. Both mRNA and protein AQP2 were significantly increased in the kidneys of the CHF rats. The effect of oral administration of a nonpeptide V2 vasopressin receptor antagonist, OPC 31260, was therefore investigated. OPC 31260 induced a significant increase in diuresis, decrease in urinary osmolality, and rise in plasma osmolality in the OPC 31260-treated CHF rats as compared to untreated CHF rats. The mRNA and protein AQP2 were significantly diminished in both cortex and inner medulla of the treated CHF rats. In conclusion, an early upregulation of AQP2 is present in CHF rats and this upregulation is inhibited by the administration of a V2 receptor antagonist. The results indicate a major role for vasopressin in the upregulation of AQP2 water channels and water retention in experimental CHF in the rat.
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              Congestive heart failure in rats is associated with increased expression and targeting of aquaporin-2 water channel in collecting duct.

              We tested whether severe congestive heart failure (CHF), a condition associated with excess free-water retention, is accompanied by altered regulation of the vasopressin-regulated water channel, aquaporin-2 (AQP2), in the renal collecting duct. CHF was induced by left coronary artery ligation. Compared with sham-operated animals, rats with CHF had severe heart failure with elevated left ventricular end-diastolic pressures (LVEDP): 26.9 +/- 3.4 vs. 4.1 +/- 0.3 mmHg, and reduced plasma sodium concentrations (142.2 +/- 1. 6 vs. 149.1 +/- 1.1 mEq/liter). Quantitative immunoblotting of total kidney membrane fractions revealed a significant increase in AQP2 expression in animals with CHF (267 +/- 53%, n = 12) relative to sham-operated controls (100 +/- 13%, n = 14). In contrast, immunoblotting demonstrated a lack of an increase in expression of AQP1 and AQP3 water channel expression, indicating that the effect on AQP2 was selective. Furthermore, postinfarction animals without LVEDP elevation or plasma Na reduction showed no increase in AQP2 expression (121 +/- 28% of sham levels, n = 6). Immunocytochemistry and immunoelectron microscopy demonstrated very abundant labeling of the apical plasma membrane and relatively little labeling of intracellular vesicles in collecting duct cells from rats with severe CHF, consistent with enhanced trafficking of AQP2 to the apical plasma membrane. The selective increase in AQP2 expression and enhanced plasma membrane targeting provide an explanation for the development of water retention and hyponatremia in severe CHF.

                Author and article information

                Nephron Physiol
                Nephron Physiology
                S. Karger AG
                July 2006
                14 July 2006
                : 103
                : 4
                : p170-p178
                Departments of aPhysiology and bInternal Medicine, Chonnam National University Medical School, Gwangju, and cDepartment of Anatomy, The Catholic Medical College, Seoul, Korea
                92918 Nephron Physiol 2006;103:p170–p178
                © 2006 S. Karger AG, Basel

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                Figures: 9, Tables: 1, References: 26, Pages: 1
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