血管紧张素Ⅱ在紧张应激引起大鼠血压升高中的作用

实验在雄性Sprague Dawley大鼠上进行。实验动物被随机分为对照组、应激组和应激 腹腔注射卡托普利 (captopril)组。应激组大鼠每天给予电击足底结合噪声的应激刺激 ,每日 2次 ,每次 2h ,连续 15d ;应激 ipcaptopril组大鼠在给予应激刺激期间 ,经腹腔内注射captopril 5 0mg/kg d。实验结果观察到 ,15d后 ,三组大鼠平均尾动脉收缩压分别为 :对照组 16 32± 0 5 5kPa (n =7) ,应激组 19 75± 1 0kPa (n =8) ,应激 ipcaptopril组17 6 9± 1 0 7kPa (n =8)。应激 ipcaptopril组大鼠的尾动脉收缩压较对照组动物有显著升高 (P <0 0 5 ) ,但又显著低于应激组大鼠 (P <0 0 5 ) ;同时 ,三组大鼠下丘脑组织中AVP mRNA水平分别为 :对照组 7332 6 6± 5 2 2 6 5 (n =6 ) ;应激组 12 990 33± 15 33 5 8(n =6 ) ,应激 ipcaptopril组 10 6 15 5± 1410 49(n =6 )。应激 ipcaptopril组大鼠下丘脑组织中AVP mRNA水平较对照组有显著升高 (P <0 0 0 1) ,但又显著低于单纯应激组大鼠 (P <0 0 5 )。统计结果显示 :各组大鼠下丘脑组织中AVP mRNA水平与血压之间存在正相关关系 (P <0 0 0 1)。对照组大鼠在侧脑室注射 (icv)选择性血管升压素 (AVP)V1受体拮抗剂d(CH2 ) 5Tyr(Me)AVP 0 3μg后 ,其平均动脉压 (

Angiotensin II participates in stress-induced high blood pressure via stimulating hypothalamic vasopressin synthesis and release

Experiments were carried out in male Sprague-Dawley rats. The animals were randomly divided into three groups: control, stressed and stress + captopril. Stress stimulations were composed of repeated electric foot-shock combined with noise, twice one day (2 h each session) for 15 consecutive days. Animals in the stress+captopril group were administered with captopril (50 mg/kg.d) intraperitoneally. The results showed that at the end of the 15-day experiment the systolic pressure of the tail artery in stressed rats was significantly higher than that of the control rats, i.e., 19.75+/ C1.0 kPa (n=8, P<0.05) versus 16.32+/ C0.55 kPa (n=7); the vasopressin (AVP) mRNA level in the hypothalamus of the stressed rats also increased significantly compared with that of the control rats, i.e., 12990.33+/ C1533.58 (n=6, P<0.001) versus 7332.66+/ C522.65 (n=6). However, in the stress + captopril rats, both the tail artery systolic pressure and hypothalamic AVP mRNA level were significantly higher than those of the control rats, but lower than those of the stressed rats. In the control rats, no significant change in mean blood pressure (MBP) was observed after intracerebroventricular (icv) injection of 0.3 microgram of d(CH(2))(5)Tyr(Me)AVP, a selective AVP V(1) receptor antagonist; however, a decrease in MBP was observed in both stressed and stress+captopril rats (P<0.05), but the decrease in stress+captopril rats was more obvious than that of the stressed rats after icv a same dose of d(CH(2))(5)Tyr(Me)AVP. These results indicate that the endogenous renin-angiotensin system participates in the mechanism of the stress-induced high blood pressure in rats, and that the effect of Ang II is mediated mainly by stimulating hypothalamic AVP synthesis and release, which in turn result in an increase in blood pressure by acting on the central V (1) receptors.