کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
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2006623 | 1066347 | 2010 | 7 صفحه PDF | دانلود رایگان |
ObjectivesThe aim of the present studywas to examine the question of whether the atrial natriuretic peptide (ANP) system is altered by endothelial nitric-oxide synthase (eNOS).MethodsMale eNOS-deficient mice (eNOS−/−) and wild type control mice (eNOS+/+, C57B1/6J) were used. Blood pressure was measured in anesthetized mice by tail cuff plethysmography and renal function was measured. Expression of ANP, natriuretic peptide receptor (NPR)-A, NPR-C, and tonicity-responsive enhancer binding protein (TonEBP) mRNA was determined by real-time PCR. Localization of 125I-ANP binding sites was measured using in vitro autoradiography.ResultsIn eNOS−/− mice, systolic blood pressure increased and left ventricular hypertrophy was observed. Urine volume and osmolarity did not change. Expression of ANP markedly increased in the heart and kidney of eNOS−/− mice. Expression of NPR-A and NPR-C increased in the heart and tended to increase in the kidney of eNOS−/− mice. In the renal medulla in particular, increased expression of NPR-C was more prominent. Expression of TonEBP mRNA was markedly decreased in the renal medulla, but not in the renal cortex. Maximum binding capacity (Bmax) of ANP and C-ANP increased in the renal medulla in eNOS−/− mice.ConclusionThese results suggest that the eNOS-NO system may be partly involved in regulation of ANP, NPR-A, -C, and TonEBP mRNA expression in the kidney.
Journal: Peptides - Volume 31, Issue 7, July 2010, Pages 1319–1325