Ismailov Sh I
Biull Eksp Biol Med. 1982 Mar;93(3):57-61.
It was shown in experiments on anesthetized normotensive, spontaneous-hypertensive rats and in those with experimental renovascular hypertension (NR, SHR and RVR, respectively) that intravenous injection of bradykinin (10 micrograms/kg) produces a decrease in arterial pressure and general peripheral vascular resistance. Intra-aortal administration of bradykinin causes hypotension as well. The degree of arterial pressure lowering in hypertensive rats is far greater than in NR. It was recorded that the cardiac component of the baroreflex to short-term aorta occlusion increases in SHR by 133% and RVR by 173%, while NR manifest its reduction by 6%. Angiotensin II (05. micrograms/kg) raises arterial pressure and general peripheral resistance, enhances pressor-reactions and potentiates reactive hyperemia. Activation of the baroreflex is recorded only in NR.
在对麻醉的正常血压大鼠、自发性高血压大鼠以及实验性肾血管性高血压大鼠(分别为NR、SHR和RVR)进行的实验中发现,静脉注射缓激肽(10微克/千克)会导致动脉血压和总外周血管阻力降低。主动脉内注射缓激肽也会引起低血压。高血压大鼠的动脉血压降低程度远大于正常血压大鼠。据记录,SHR中对短期主动脉闭塞的压力反射的心脏成分增加了133%,RVR中增加了173%,而NR中则降低了6%。血管紧张素II(0.5微克/千克)会升高动脉血压和总外周阻力,增强升压反应并增强反应性充血。仅在NR中记录到压力反射的激活。