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目的探讨厄贝沙坦对肾性高血压大鼠(RHR)血管Na+-K+-腺苷三磷酸酶(ATPase)、Ca2+-ATPase和血管紧张素Ⅱ(AngⅡ)及血管重塑的影响。方法采用两肾一夹制造肾血管性高血压大鼠模型,18只造模成功的大鼠随机分为RHR组、厄贝沙坦组[50 mg/(kg.d)]、停药组[厄贝沙坦50 mg/(kg.d)灌胃7周后停药1周],每组6只。另设一假手术组(n=6)。测量各组大鼠用药前后血压;8周后,测量大鼠胸主动脉及肠系膜动脉血管壁厚度;采用酶学比色法检测Na+-K+-ATPase、Ca2+-ATPase活性;采用放射免疫技术检测血浆、肠系膜动脉及胸主动脉局部AngⅡ水平。结果与假手术组比较,RHR血压显著升高,血管壁厚度明显增厚,血浆及血管组织AngⅡ明显升高,血管Na+-K+-ATPase、Ca2+-ATPase活性降低;与RHR组比较,厄贝沙坦组大鼠血压明显降低,肠系膜动脉血管壁厚度明显减轻,胸主动脉、肠系膜动脉AngⅡ水平及Ca2+-ATPase活性均升高,Na+-K+-ATPase活性无明显变化;与厄贝沙坦组比较,停药组血压明显升高,胸主动脉及肠系膜动脉Ca2+-ATPase活性明显降低,Na+-K+-ATPase活性无变化。RHR血管Ca2+-ATPase活性与局部AngⅡ呈负相关。结论RHR血管重塑与血管组织ATPase活性降低、AngⅡ升高有关,厄贝沙坦逆转血管重塑的作用可能部分与Ca2+-ATPase活性增加有关。
Objective To investigate the effects of irbesartan on the expressions of Na + -K + -ATPase, Ca2 + -ATPase and angiotensin Ⅱ (AngⅡ) and vascular remodeling in renovascular hypertensive rats (RHR). Methods Renal vascular hypertensive rat model was established by two kidneys and one clip. Eighteen rats were randomly divided into RHR group, irbesartan group [50 mg / (kg · d)], withdrawal group [ Irbesartan 50 mg / (kg.d) for 7 weeks after gavage for 1 week], 6 in each group. Another set of sham operation group (n = 6). The blood pressure of rats in each group was measured before and after treatment. After 8 weeks, the thoracic and mesenteric artery wall thickness were measured. The activities of Na + -K + -ATPase and Ca2 + -ATPase were detected by enzyme-linked immunosorbent assay (ELISA) , Mesenteric artery and thoracic aorta Ang Ang level. Results Compared with the sham-operation group, the blood pressure of RHR increased significantly, the thickness of blood vessel wall increased obviously, the Ang Ⅱ level in blood plasma and blood vessel increased significantly, and the activity of Na + -K + -ATPase and Ca2 + -ATPase decreased. Compared with RHR group, The blood pressure of the rats in the Tan group was significantly decreased, the thickness of the mesenteric artery vessel wall was significantly reduced, the AngⅡ level and Ca2 + -ATPase activity in the thoracic aorta and mesenteric artery were elevated, and the Na + -K + -ATPase activity was unchanged. Compared with irbesartan group , The blood pressure in the withdrawal group was significantly increased, the activities of Ca2 + -ATPase in the thoracic aorta and mesenteric artery were significantly decreased, and the activity of Na + -K + -ATPase was unchanged. The activity of Ca2 + -ATPase in RHR was negatively correlated with AngⅡ. Conclusions The angiogenesis remodeling of RHR is related to the decrease of ATPase activity and the increase of Ang II in vascular tissue. The effect of irbesartan on vascular remodeling may partly be related to the increase of Ca2 + -ATPase activity.