Interaction of sodium loading and enalapril on renin mRNA and renin release in hydronephrotic mice.
- Author:
Yan-Ling ZHANG
1
,
2
;
Jun-Yan WU
;
Xue-Chun WANG
;
Lei LIU
Author Information
1. Department of Fundamental Medicine
2. Taishan Medical University, Taian, China. zyl@tsmc.edu.cn
- Publication Type:Journal Article
- MeSH:
Animals;
Aorta;
metabolism;
Enalapril;
pharmacology;
Hydronephrosis;
metabolism;
Kidney;
physiopathology;
Mice;
Mice, Inbred BALB C;
RNA, Messenger;
metabolism;
Renin;
metabolism;
Renin-Angiotensin System;
drug effects;
Sodium;
metabolism
- From:
Acta Physiologica Sinica
2009;61(3):239-246
- CountryChina
- Language:English
-
Abstract:
The present study investigated the interaction between sodium loading and enalapril on renin synthesis and secretion in hydronephrotic mice. Four different experimental groups (n=10 each) were used: sham-operated animals with normal diet (control group); sodium loading (SL group); enalapril treatment with normal diet (E group), and sodium loading combined with enalapril treatment (SL+E group). The hydronephrotic left kidney was induced by unilateral ureteral ligation in mice in the latter three groups. Plasma renin concentration (PRC) in the aorta, both the left and right renal veins, tissue renin concentration (TRC) and renin mRNA levels in the kidneys were examined under different procedures. In hydronephrotic mice treated with sodium loading, PRC in the left and right renal veins was lower than that in control mice (P<0.05), and TRC and renin mRNA levels in the hydronephrotic kidney were also suppressed (P<0.05). In hydronephrotic mice treated with enalapril, there were significant increases in PRC, TRC and renin mRNA levels in the hydronephrotic and right kidneys compared to the normal control (P<0.01). In hydronephrotic animals treated with sodium loading and enalapril, the increasing response was attenuated, and PRC in the hydronephrotic vein was similar to the level in the aorta. There was an interaction between sodium loading and enalapril on renin-angiotensin system (RAS) in both hydronephrotic and normal kidneys. The mechanism in control of renin synthesis is independent of the macula densa, but the latter is critical in the control of renin secretion.
