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Increased expression of atrial natriuretic peptide in the kidney of rats with bilateral ureteral obstruction. Background. Whether the postobstructive diuresis can be related to an altered regulation of local atrial natriuretic peptide (ANP) in the kidney was investigated. Methods. Three groups of rats had both of their ureters obstructed for 48 hours. The kidneys were taken without releasing the obstruction in one group [bilateral ureteral obstruction (BUO)]. The obstruction was released in the other two groups and the animals were kept for 4 and 24 hours thereafter to collect urinary data (BUR-4 and BUR-24, respectively). Plasma and urine ANP levels were measured by radioimmunoassay. The mRNA expression of ANP, natriuretic peptide receptor-A (NPR-A), and NPR-C was determined by reverse transcription-polymerase chain reaction. ANP receptors were also quantitated by in vitro autoradiography. The activity of guanylyl cyclase was determined by the amount of cGMP generated in response to ANP. Results. Urinary volume and sodium excretion increased in BUR-4, along with the ANP mRNA expression in the kidney and the urinary ANP excretion. The ANP excretion positively correlated with the urinary volume and sodium excretion. The mRNA expression of both NPR-A and NPR-C was decreased by BUO, the latter being far more prominently affected. The maximal binding capacity of radiolabeled ANP was decreased in the glomerulus and papilla in BUO. Not only the urinary parameters but also the mRNA expression of ANP, NPR-A, and NPR-C were comparable between BUR-24 and control rats. ANP-stimulated cGMP generation was reduced in the glomerulus and papilla in BUO animals, which was rapidly resumed following the release of the obstruction. Conclusions. Postobstructive diuresis may be due partially to an increased ANP activity in the kidney. [ABSTRACT FROM AUTHOR]

Abstract: The present study was aimed to determine whether there is an altered role of local nitric oxide (NO) and atrial natriuretic peptide (ANP) systems in the kidney in association with the angiotensin (Ang) II-induced hypertension. Male Sprague–Dawley rats were used. Ang II (100ng·min−1·kg−1) was infused through entire time course. Thirteenth day after beginning the regimen, kidneys were taken. The protein expression of NO synthase (NOS) and nitrotyrosine was determined by semiquantitative immunoblotting. The mRNA expression of components of ANP system was determined by real-time polymerase chain reaction. The activities of soluble and particulate guanylyl cyclases were determined by the amount of cGMP generated in responses to sodium nitroprusside and ANP, respectively. There developed hypertension and decreased creatinine clearance in the experimental group. The protein expression of eNOS, nNOS and nitrotyrosine was increased in the cortex, while that of iNOS remained unaltered. The urinary excretion of NO increased in Ang II-induced hypertensive rats. The catalytic activity of soluble guanylyl cyclase was blunted in the glomerulus in Ang II-induced hypertensive rats. The mRNA expression of ANP was increased in Ang II-induced hypertensive rats. Neither the expression of NPR-A nor that of NPR-C was changed. The protein expression of neutral endopeptidase was decreased and the activity of particulate guanylyl cyclase was blunted in the glomerulus and papilla in Ang II-induced hypertensive rats. In conclusion, the synthesis of NO and ANP was increased in the kidney of Ang II-induced hypertension, while stimulated cGMP response was blunted. These results suggest desensitization of guanylyl cyclase in the kidney of Ang II-induced hypertensive rats, which may contribute to the associated renal vasoconstriction and hypertension. [Copyright &y& Elsevier]

Abstract: The present study was aimed to determine whether there is an altered role of local nitric oxide (NO), atrial natriuretic peptide (ANP) and cyclooxygenase (COX) systems in the kidney in association with the aldosterone escape. Male Sprague–Dawley rats were used. Aldosterone (200μg/day) was infused through entire time course. The control group was kept on a low sodium diet (0.02mEq/day), and the experimental group was supplied with a higher sodium diet (2.0mEq/day). Four days after beginning the regimen, the kidneys were taken. The protein expression of NO synthase (NOS) and COX isoforms was determined by semiquantitative immunoblotting. The mRNA expression of components of ANP system was determined by real-time polymerase chain reaction. The activities of soluble and particulate guanylyl cyclases were determined by the amount of cGMP generated in responses to sodium nitroprusside and ANP, respectively. There developed aldosterone escape in the experimental group. Accordingly, the renal content and the urinary excretion of NO increased. The expression of nNOS was increased in the inner medulla. Neither the expression of eNOS nor that of iNOS was changed. The expression and the catalytic activity of soluble guanylyl cyclase remained unaltered. The mRNA expression of ANP was increased. Neither the expression of NPR-A or NPR-C nor the activity of particulate guanylyl cyclase was altered in the papilla. The protein expression of COX-2 was increased in the inner medulla, while that of COX-1 remained unchanged. In conclusion, the upregulation of nNOS, ANP, and COX-2 may be causally related with the aldosterone escape. [Copyright &y& Elsevier]