Superimposing a high-fat diet on schistosoma mansoni infection affects renin-angiotensin system components in the mouse kidney

Abstract INTRODUCTION: The levels of the full-length form of the (pro)renin receptor (PRR), a component of the renin-angiotensin system (RAS), may be reduced in the membranes of kidneys in renal diseases. This study aimed to investigate the RAS components in the kidneys of mice submitted to a combination of a high-fat diet and Schistosoma mansoni infection. METHODS: Female BALB/c mice were maintained on a control or high-fat diet from 3 weeks of age. After 10 weeks on the designated diets, half the mice in each group were infected with S. mansoni cercariae. The blood and kidneys were harvested 8 weeks after infection. RESULTS: The high-fat diet increased the number of eggs in the feces and the number of adult worms in the mesenteric bed. Schistosoma mansoni infection reduced the plasma levels of glucose, triglycerides, and HDL cholesterol in the control and high-fat diet groups. In mice on the control diet, S. mansoni infection resulted in increased expression of IL-6 in the kidneys; however, in mice on the high-fat diet, the levels of IL-6 were reduced and those of superoxide anions were increased. The RAS components evaluated were ACE2, renin, PRR, AT1R, and AT2R, and the levels of PRR were found to be reduced in the kidneys of infected mice on the high-fat diet. CONCLUSIONS: The finding regarding PRR is not yet clear. However, combining a high-fat diet and S. mansoni infection resulted in increased oxidative stress in the kidney that can aggravate hypertension as well as its associated complications.

(Pro)Renin Receptor as a Novel Mediator of Renal Handling of Fluid and Electrolytes / 中山大学学报(医学科学版)

(Pro)renin receptor(PRR)was organically identified as a specific receptor for prorenin and renin to regulate the activity of renin-angiotensin system(RAS). Increasing evidence suggests that PRR plays a multitude functions in a RAS-dependent and independent manner. The extracellular domain of PRR is cleaved by furin or ADAM19 to produce a 28-ku soluble PRR(sPRR) while the intracellular domain,M8.9,is a subunit of vacuolar H+-ATPase that mediates H+transport. PRR is critically involved in embryogenesis in low vertebrates and mammals. In recent years ,a significant progress has been made in identifying the physiological and pathophysiological functions of renal PRR. PRR has been identified as an important regulator of urine concentrating capability mostly due to its ability to upregulate to aquaporin-2(AQP2)in the collecting duct and Na+,K+,2Cl-cotransporter(NKCC2)in the thick ascending limb. PRR also promotes K+ secretion in response to K+loading through extra-adrenal aldosterone(Aldo)produc?tion. Overactivation of renal PRR contributes to the pathogenesis of hypertension induced by angiotensin Ⅱ infusion and fructose/salt. Overall,PRR has emerged as a new regulator of physiological and pathophysiological processes in the kidney.

(Pro)renin receptor in heart disease / 国际儿科学杂志

The renin-angiotensin system is an important body fluid regulation system in the human body,and it normally plays a significant role in the normal development and homeostatic regulation of the cardio-vascular system,the maintenance of electrolyte and body fluid balance,and the regulation of blood pressure.The (pro)renin receptor[(P)RR ] was been discovered as an important novel component of the renin-angiotensin system.It binds both prorenin and renin in tissues.(P)RR is widely expressed in human body,including kidney, brain,heart and placenta.It has been proved that the activated(P)RR participates in the activation of multiple in-tracellular signaling pathways and plays an important role in the pathogenesis of diabetic complications,hyperten-sion,heart failure and myocardial fibrosis.This review mainly summarizes the research progress of expression and function of(pro)renin receptor in the heart.

Establishment of Cardio-renal Syndrome and the mRNA Expression of Pro-renin Receptor in Experimental Rat’s Model / 中国循环杂志

Objective: To establish the cardio-renal syndrome (CRS) model by coarctation of abdominal aorta (CAA) with renal ischemia reperfusion injury (RIRI), and to observe the mRNA expression of pro-renin receptor [(P)RR] in experimental rats. Methods: A total of 42 Wistar rats were randomly divided into 4 groups: Sham group, CAA group, RIRI group and CAA+RIRI group.n=10 in each group, 2 rats died during the modeling and all animals were treated for 16 weeks. Blood levels of BNP, creatinine (Cr), urea nitrogen (BUN), the activity of rennin, the contents of angiotensin-I (AT-I), AT-II and aldosterone were examined by laboratory test. The diastolic end inter-ventricular septum thickness (DEIVST), DELVPT, LVEF, ventricular weight index (VWI) and cardiac weight index were detected by small animal echocardiography. The histological changes of myocardium and kidney tissue were measured by HE staining, and the mRNA expressions of pro-renin receptor in myocardium and kidney tissues were measured by RT-PCR. Results: Compared with Sham group, blood levels of BNP were increased in the other 3 groups,P0.05. Compared with CAA group, CAA+RIRI group had more obvious changes of DEIVST and LVEF,P<0.01. Compared with RIRI group, CAA+RIRI group had more obvious ventricular hypertrophy, higher VWI and cardiac weight index, allP<0.05. HE staining presented that CAA+RIRI group had broadening of myocardial cell bundle space, decreased left renal index, severe tubular atrophy and partial glomerular atrophy. RT-PCR demonstrated that compared with Sham group, the mRNA expressions of pro-renin receptor in myocardium and kidney tissues were decreased in the other 3 groups. Conclusion: Combined CAA+RIRI method may damage the cardial and renal tissues at the same time which was more severe than either CAA or RIRI. While CAA+RIRI model has better controllability and higher consistency that provides a methodological reference for pro-renin receptor in treating CRS in experimental rat’s model.