Abstract：
OBJECTIVES:The 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). METHODS:Male 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 (125)I-ANP binding sites was measured using in vitro autoradiography. RESULTS:In 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 (B(max)) of ANP and C-ANP increased in the renal medulla in eNOS-/- mice. CONCLUSION:These 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_name
Peptidesjournal_title
Peptidesauthors
Yuan K,Kim SY,Oh YB,Yu J,Shah A,Park BH,Kim SHdoi
10.1016/j.peptides.2010.04.008subject
Has Abstractpub_date
2010-07-01 00:00:00pages
1319-25issue
7eissn
0196-9781issn
1873-5169pii
S0196-9781(10)00162-2journal_volume
31pub_type
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