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GW24-e3524 PARTIAL AORTIC CONSTRICTION IN RATS INCREASES THE EXPRESSION OF (PRO)RENIN RECEPTOR AND PLC-b3 IN THE HEART
  1. Yanling Zhang1,
  2. Lulu Ma1,
  3. Junyan Wu1,
  4. Trefor Morgan2
  1. 1Department of Physiology, Taishan Medical University, Taian, China
  2. 2Department of Physiology, The University of Melbourne, Vic, Australia

Abstract

Objectives Recent studies have shown that (pro)renin receptor (P)RR), a newly identified member of the renin-angiotensin system, was associated with organ damage in the kidney. However, there has been less information for (P)RR) in the heart. To investigate the regulation of (P)RR) and its signal transduction mechanism in cardiac hypertrophy we examined the expression of (P)RR) and PLC-b3 in the heart of rats with renovascular hypertension due to abdominal aortic ligation by RT-PCR and Western blot.

Methods Forty SD rats were divided into 4 groups (10 rats in each group) as following: sham operated (SO), rats with the aortic ligation (AL), AL rats were given HRP (4 µg kg-1 d-1, SC), and AL rats given U73122 (40 µg kg-1 d-1, SC). MAP was recorded using a tail-cuff method. After 4 weeks of treatment, levels of (P)RR) and PLC-b3 in the heart were examined by RT-PCR and western blot. Plasma renin activity (PRA) was measured by radioimmunoassay.

Results Significantly increased levels of (P)RR) and PLC-b3 mRNAs were found in the left and right ventricles of hypertensive rats, when compared with sham operated rats (1.3-fold and 1.6-fold, P < 0.01, respectively). There was similar percentage of changes in both protein levels. HRP treatment significantly reduced the expression of (P)RR) while U73122 suppressed the level of PLC-b3 in the heart. There is a correlation between changes in the expression of (P)RR) and PLC-b3.

Conclusions The data showed that the effects of HRP and U73122 on the expression of (P)RR) and PLC-b3 in the heart. These findings suggest that the expression of cardiac (P)RR) is increased in rats with hypertension and PLC-b3 may involve in the signal transduction of (P)RR) leading to cardiac hypertrophy.

Acknowledgement This study was supported by the National Natural Science Foundation of China (81270336).

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