EFFECTS OF SARALASIN ON ARTERIAL COMPLIANCE IN NORMOTENSIVE AND HYPERTENSIVE RATS - ROLE OF ENDOTHELIUM

We used an experimental model of in situ isolated carotid arteries to clarify the participation of angiotensin II (Ang II) in the mechanical properties of the arterial wall in 12-week-old Wistar-Kyoto (WKY) and spontaneously hypertensive rats (SHRs). The effects of local incubation with saralasin ([Sar1,Thr8]Ang II, 10(-6) M) on carotid compliance were compared with the effects of endothelium removal and with those of total abolition of vasomotor tone with potassium cyanide (0.1 mg/ml). Operating carotid compliance measured for pressure values close to the mean arterial pressure of each group was (mean +/- SD) 12.6 +/- 2.9 x 10(-3)-mu-l/ mm Hg . mm vessel in WKY rats and 8.2 +/- 1.6 x 10(-3)-mu-l/mm Hg . mm vessel in SHRs (p < 0.001). With intact endothelium, local incubation with saralasin increased carotid compliance by 24% in WKY rats and 23% in SHRs relative to control values (p < 0.05 and p < 0.001, respectively). Endothelium removal induced significant increases in carotid compliance in WKY rats (17%, p < 0.01) and in SHRs (33%, p < 0.001). After endothelium removal, saralasin induced significant further carotid compliance increases in both strains (+ 18%, p < 0.001, and + 11%, p < 0.01, in WKY rats and SHRs, respectively). After potassium cyanide poisoning, carotid compliance did not increase further relative to saralasin values in both strains with or without endothelium. These findings suggest that Ang 11 receptors play a major role in the control of the 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 inhibitors could involve similar mechanisms on the smooth muscle angiotensin receptors.