Sclederma of Poria cocos exerts its diuretic effect via suppression of renal aquaporin-2 expression in rats with chronic heart failure.

ETHNOPHARMACOLOGICAL RELEVANCE: Sclederma of Poria cocos (Hoelen) has been used as a diuretic in traditional Asian medicine. However, the underlying mechanism by which Sclederma of Poria cocos (hoelen) exerts its diuretic effect has not been well identified. The aim of the present study was to evaluate the effects of Sclederma of Poria cocos (hoelen) in rats with chronic heart failure (CHF) induced by acute myocardial infarction and to investigate the underlying mechanisms. MATERIALS AND METHODS: An aqueous extract of Sclederma of Poria cocos (hoelen) (2.4 g/kg/d, 1.2 g/kg/d or 0.6 g/kg/d) or furosemide (20 mg/kg/d) was administered orally to male Sprague-Dawley rats starting on the day of coronary ligation. The urine output of all rats was quantified and collected every day for 1 or 4 weeks. The expression of aquaporin-2 (AQP2) was examined after treatment for 1 or 4 weeks. RESULTS: Urinary output increased significantly and urinary osmolality decreased after oral administration of Sclederma of Poria cocos (hoelen) for both 1 and 4 weeks. Sclederma of Poria cocos (hoelen) caused less electrolyte disorder than furosemide. Furthermore, Sclederma of Poria cocos (hoelen) reduced the levels of plasma BNP in CHF rats, whereas furosemide had no effect. Importantly, both mRNA and protein expression of AQP2 were down-regulated and urinary excretion of AQP2 was decreased after administration of Sclederma of Poria cocos (hoelen) to CHF rats. Similarly, Sclederma of Poria cocos (hoelen) reduced plasma arginine vasopressin (AVP) level and down-regulated vasopressin type 2 receptor (V2R) mRNA expression. CONCLUSIONS: Sclederma of Poria cocos (hoelen) exerts its diuretic effect and improves cardiac function in CHF rats via the AVP-V2R-AQP2 axis.

[Value of C-reactive protein in the diagnosis of arteriosclerosis in patients with essential hypertension].

OBJECTIVE: To evaluate the value of C-reactive protein (CRP) in the diagnosis of arteriosclerosis in patients with essential hypertension. METHODS: This study included 771 patients with essential hypertension and 243 healthy individuals, and all the subjects were measured for carotid-femoral pulse wave velocity (cfPWV) and serum CRP level using enzyme-linked immunosorbent assay (ELISA). The value of CRP in the diagnosis of arteriosclerosis in patients with essential hypertension was evaluated according to the receiver operating characteristics (ROC) curve, and the diagnostic sensitivity and specificity was evaluated with cfPWV> or =9 m/s as the golden diagnostic standard. RESULTS: The hypertensive patients had significantly higher cfPWV and serum CRP concentration than the healthy individuals (16.51-/+1.6 vs 9.81-/+1.1, P<0.001; 4.96-/+1.15 vs 3.52-/+0.33, P<0.001, respectively). CRP showed significant positive correlations to systolic blood pressure (SBP) and pulse pressure (PP) (r=0.584, P<0.001; r=0.624, P<0.001), and when controlled for age, SBP and PP, CRP was found in close correlation to cfPWV (r=0.746, P<0.001). The AUCROC of CRP was 0.907, and the peak point of the ROC curve was 3.85 mg/L, at which point CRP showed a diagnostic sensitivity of 83.9% and specificity of 86.8% with a misdiagnosis rate of 13.2% for arteriosclerosis. CONCLUSIONS: Arteriosclerosis and nonspecific inflammation are prevalent in patients with essential hypertension, and CRP with the cutoff value of 3.85 mg/L may serve as a sensitive indicator for arteriosclerosis diagnosis in these patients.

[Effects of losartan on left ventricular hypertrophy and plasma transforming growth factor-beta1 in elderly patients with hypertension].

OBJECTIVE: To investigate the effects of losartan on left ventricular hypertrophy (LVH) and plasma transforming growth factor-beta1 (TGF-beta1) in elderly patients with essential hypertension (EH). METHODS: The elderly patients with EH were divided into two groups, namely EH+LVH group and EH group according to the data of echocardiogram. The systolic and diastolic blood pressures of the patients were monitored. Plasma TGF-beta1 was measured before and after 6 months' treatment with losartan, and the relationship between TGF-beta1 and other index were analyzed. RESULTS: After 6 months' treatment, the blood pressure of EH+LVH group and EH group were significantly lowered (P<0.01). Significant improvement of IVSTd, LVPWd, E/A, and LVMI (P<0.01) and obvious reduction of plasma TGF-beta1 (P<0.01) occurred in EH+LVH group after 6 months' treatment. Correlation analyses indicated that the plasma TGF-beta1 level was positively correlated to LVMI (P<0.01). CONCLUSION: Losartan can reversed LVH in elderly patients with EH partially by lowering plasma TGF-beta1 level.

[Mechanisms of losartan for inhibition of myocardial fibrosis following myocardial infarction in rats].

OBJECTIVE: To investigate the effect of losartan on cardiac mineralocorticoid receptor (MR) mRNA in rats after acute myocardial infarction (AMI). METHOD: AMI was induced in male SD rats by ligation of the left coronary artery. The survived rats were randomly divided into AMI group, losartan group, and sham-operated group. The cardiac functions of the rats were assessed by echocardiogram and hemodynamics, and the contents of angiotensin II (Ang II) and aldosterone (Ald) in the myocardial tissues were determined by radioimmunoassay. The collagen density in the myocardial tissues were calculated by Masson's trichrome staining and the expression of MR mRNA were determined by real-time quantitative fluorescent PCR. RESULTS: Both the contents of AngII and Ald in the myocardial tissues increased significantly in AMI group compared with those in the sham-operated group (P<0.01). The expression of MR mRNA and collagen density in the myocardial tissues also increased significantly than that in sham-operated group (P<0.01). After four weeks of losartan treatment, the contents of AngII and Ald in the myocardial tissues decreased significantly (P<0.05) and the expression of MR mRNA was also considerably lowered (P<0.01) in comparison with those in the AMI group. Treatment with losartan also resulted in significant decrease of the collagen density in the myocardial tissues. CONCLUSIONS: Losartan may reduce reactive fibrosis not only by attenuating the Ald signaling pathway but also by decreasing the expression of MR.