Levy B I, Stefas L, Babalis D, Benetos A
Institut National de la Santé et de la Recherche Médicale, Hôpital Lariboisière, Paris, France.
J Hypertens Suppl. 1992 Jul;10(5):S21-7.
An experimental model of in situ isolated carotid arteries was used to study the contribution made by angiotensin II (Ang II) towards the mechanical properties of the arterial wall in 12-week-old Wistar-Kyoto (WKY) and spontaneously hypertensive (SHR) rats. The effects of local incubation with saralasin (Sar1-Thr8-Ang II, 10(-6) mol/l) and with lisinopril (5 x 10(-6) mol/l) on carotid compliance were compared to the effects of removing the endothelium and the effects of totally abolishing vasomotor tone with potassium cyanide (0.1 mg/ml).
With an intact endothelium, local incubation with lisinopril increased carotid compliance by 23% in WKY rats (P less than 0.05) and by 14% in SHR (P less than 0.01). Under the same experimental conditions, saralasin increased carotid compliance by 24% in WKY rats and 23% in SHR relative to control values (P less than 0.05 and P less than 0.001, respectively). Removal of the endothelium induced significant increases in carotid compliance in WKY rats (17%, P less than 0.01) and in SHR (33%, P less than 0.001). After removal of the endothelium, there was no further increase in carotid compliance with lisinopril in either strain. In contrast, saralasin induced further significant compliance increases in both strains (+18%, P less than 0.001, and +11%, P less than 0.01, in WKY and SHR, respectively). After the artery had been poisoned with potassium cyanide, there was no further increase in compliance relative to values obtained with saralasin in either strain with or without the endothelium.
These findings suggest that Ang II receptors have a major effect on the control of basal vasomotor tone of large arteries in both normotensive and hypertensive rats. Furthermore, the increase in carotid compliance induced by local incubation with saralasin and with angiotensin converting enzyme (ACE) inhibitors may involve similar mechanisms acting on smooth muscle angiotensin receptors.
采用原位分离颈动脉实验模型,研究血管紧张素II(Ang II)对12周龄Wistar - Kyoto(WKY)大鼠和自发性高血压(SHR)大鼠动脉壁力学特性的影响。将局部孵育沙拉新(Sar1 - Thr8 - Ang II,10⁻⁶ mol/L)和赖诺普利(5×10⁻⁶ mol/L)对颈动脉顺应性的影响,与去除内皮的影响以及用氰化钾(0.1 mg/ml)完全消除血管运动张力的影响进行比较。
在内皮完整的情况下,局部孵育赖诺普利使WKY大鼠的颈动脉顺应性增加23%(P < 0.05),使SHR大鼠的颈动脉顺应性增加14%(P < 0.01)。在相同实验条件下,相对于对照值,沙拉新使WKY大鼠的颈动脉顺应性增加24%,使SHR大鼠的颈动脉顺应性增加23%(分别为P < 0.05和P < 0.001)。去除内皮导致WKY大鼠(17%,P < 0.01)和SHR大鼠(33%,P < 0.001)的颈动脉顺应性显著增加。去除内皮后,两种品系的大鼠使用赖诺普利均未使颈动脉顺应性进一步增加。相比之下,沙拉新使两种品系的大鼠颈动脉顺应性进一步显著增加(WKY大鼠增加18%,P < 0.001;SHR大鼠增加11%,P < 0.01)。在用氰化钾使动脉中毒后,无论有无内皮,两种品系大鼠相对于用沙拉新获得的值,顺应性均未进一步增加。
这些发现表明,Ang II受体对正常血压和高血压大鼠大动脉基础血管运动张力的控制有主要影响。此外,局部孵育沙拉新和血管紧张素转换酶(ACE)抑制剂诱导的颈动脉顺应性增加可能涉及作用于平滑肌血管紧张素受体的类似机制。