Oleanolic Acid Prevents Increase in Blood Pressure and Nephrotoxicity in Nitric Oxide Dependent Type of Hypertension in Rats.
Oleanolic Acid Prevents Increase in Blood Pressure and Nephrotoxicity in Nitric Oxide Dependent Type of Hypertension in Rats.
复制标题
DOI：
10.4103/0974-8490.159575
复制
发表时间：
2014-10
影响因子：
0.7
通讯作者：
Patil SD
中科院分区：
文献类型：
--
作者：
Bachhav SS;Bhutada MS;Patil SP;Sharma KS;Patil SD
最近，我们报道了油酸（OA）在糖皮质激素诱导的高血压中的降压活性，并恢复一氧化氮（NO）水平。然而，OA的NO释放作用的参与尚不清楚。探讨OA对一氧化氮（NO）完全阻断的Nω-硝基-L-精氨酸甲酯（L-NAME）高血压大鼠的降压作用，探讨OA参与NO释放作用的可能性。实验分为正常对照组、L-NAME（40 mg/kg/d）组、L-NAME +依那普利（15 mg/kg/d）组、L-NAME + L-精氨酸（100 mg/kg/d）组和L-NAME + OA（60 mg/kg/d）组，共4周。每周测量收缩压、体重和心率，持续4周。测定血清硝酸盐/亚硝酸盐（NOx）水平、尿电解质浓度、心脏质量指数和血清肌酐水平，然后进行器官组织病理学检查。OA和依那普利推迟了L-NAME给药后血液快感的上升。任何治疗均未显著增加降低的血清NOx水平。OA产生了一个小的，但不显着，增加氮氧化物水平。L-NAME给药不影响心脏质量指数。L-NAME给药后血清肌酐升高，但OA可预防。尿量、尿钠和尿钾的减少可被OA逆转。这些结果表明，OA在L-NAME高血压中的降压作用是由于利尿和肾保护作用。然而，OA对NO水平无显著影响。
Recently, we have reported antihypertensive activity of oleanolic acid (OA) in glucocorticoid-induced hypertension with restoration of nitric oxide (NO) level. However, the involvement of NO-releasing action of OA was unclear. To explore antihypertensive activity of OA in Nω-nitro-L-arginine methyl ester (L-NAME) hypertensive rats wherein NO is completely blocked, which would allow exploring the possibility of involvement of NO-releasing action of OA. Five groups of rats were investigated as normal control, L-NAME (40 mg/kg/day), L-NAME + enalapril (15 mg/kg/day), L-NAME + l-arginine (100 mg/kg/day), and L-NAME + OA (60 mg/kg/day) for 4 weeks. The systolic blood pressure, body weight, and heart rate were measured weekly for 4 weeks. Serum nitrate/nitrite (NOx) level, urine electrolytes concentration, cardiac mass index, and serum creatinine level were determined followed by organ histopathology. OA and enalapril delayed the rise in blood pleasure following L-NAME administration. Decreased serum NOx level was not significantly increased with any of the treatment. OA produced a small, though nonsignificant, increase in the NOx level. L-NAME administration did not affect cardiac mass index. There was an increase in serum creatinine upon L-NAME administration which was prevented by OA. Decreased urine volume, urine sodium and potassium were reversed by OA. These results suggest that the antihypertensive effect of OA in L-NAME hypertension is due to diuresis and nephroprotection. However, OA has nonsignificantly affected the NO levels.