Vascular endothelium, mechanical properties of the arterial wall and local angiotensin converting enzyme inhibition

Abstract

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.