Journal of the Renin-Angiotensin-Aldosterone System最新文献

Autoregulation of cerebral blood flow (CBF) denotes that CBF is constant despite fluctuation of blood pressure within wide limits. Inhibition of the renin-angiotensin system (RAS) is known to decrease the lower and upper limits of CBF autoregulation. We have previously shown that this includes inhibition by the angiotensin receptor blocker (ARB) candesartan. In the present study we investigated the influence of the ARB candesartan on the lower limit of CBF autoregulation in two groups of Sprague-Dawley rats, on high (4.0% Na⁺) and low (0.004% Na⁺) sodium diet, respectively. Control animals were given the same diet, but no ARB. CBF was studied with the laser Doppler method. Blood pressure was lowered by controlled bleeding. Results revealed that both high and low sodium diet with low and high renin levels respectively block the influence of candesartan on CBF autoregulation. This was expected in rats on a high salt diet with a low renin level, but unexpected in rats with a low salt intake with a high renin level.

Introduction: Bone marrow renin-angiotensin system(RAS) modulates acute myeloid leukaemia(AML).The aim of this study is to clarify the relationships between RAS and AML, and to show the effect of losartan and doxorubicin treatment in AML cell lines.

Methods: AML cell lines including CESS, HL-60, MO-1, P31/FUJ, GDM-1 and KASUMI-3 were used as models in this study.

Results: After treating the six AML cell lines with a combination of losartan and doxorubicin, they were divided into two groups based on their behaviour: one became more sensitive to drug treatment (Group A) and the other had no change observed in behaviour after drug treatment (Group B). In silico analyses showed that Group A is involved in cellular apoptosis, while Group B is involved in tumour angiogenesis further supporting the in vitro results.

Conclusion: The combined treatment of the AML cell lines with losartan and doxorubicin resulted in an increase in sensitivity of some of the cell lines. Those leukaemic cells are modulated via the induction of apoptosis, whereas the other cells resistant to the drug treatment are closely related to tumour angiogenesis indicating that RAS-AT1R seems to be differently expressed in different leukaemic blast cells and tumour microenvironments. Pharmaco-biological actions of RAS inhibitors may be different in distinct leukaemic cells based on the pathological behaviour of AML genomic subtypes.

Objective:: Meta-analysis was performed in the current study to evaluate the relationship of the angiotensin-converting enzyme insertion/deletion polymorphism with the risk of the incidence of Henoch-Schönlein purpura.

Methods:: The electronic databases, including Embase, PubMed and Google scholar, were systemically retrieved to search for related articles. Meanwhile, statistical analysis was performed using the odds ratio and the corresponding 95% confidence interval.

Results:: A total of six articles enrolling 504 patients and 706 healthy controls was enrolled into the current meta-analysis. Results of the meta-analysis suggested that the angiotensin-converting enzyme D allele was markedly correlated with the risk of the incidence of Henoch-Schönlein purpura among the general population (deletion (D) vs. insertion (I): odds ratio (OR) 1.42, 95% confidence interval (CI) 1.05-1.93; DD vs. II: OR 2.23, 95% CI 1.06-4.70; DI vs. II: OR 1.36, 95% CI 1.00-1.85; dominant model: OR 1.56, 95% CI 1.00-2.42; recessive model: OR 1.83, 95% CI 1.06-3.16). Moreover, such a polymorphism was found to correlate with the susceptibility to Henoch-Schönlein purpura when studies were stratified according to the sample size of over 200. In addition, such a polymorphism was recognised to be remarkably associated with the susceptibility to Henoch-Schönlein purpura in the Caucasian population, which was not found in the Asian population.

Conclusions:: The results of the current meta-analysis indicate that the angiotensin-converting enzyme D allele might be a risk factor against the risk of Henoch-Schönlein purpura, especially in Caucasians.