O'Sullivan J B, Black M J, Bertram J F, Bobik A
Baker Medical Research Institute, University of Melbourne, Australia.
J Hypertens. 1994 Oct;12(10):1163-70.
To investigate the role of angiotensin II (Ang II) in cardiovascular hypertrophy in the Goldblatt one-kidney, one clip (1-K, 1C) renal hypertensive rat.
Six-week-old Wistar-Kyoto (WKY) rats underwent uninephrectomy and left renal artery clipping. After surgery, rats were treated with perindopril, an angiotensin converting enzyme (ACE) inhibitor, or losartan, an Ang II type 1 (AT1) receptor antagonist, for 4 weeks. Untreated 1-K, 1C rats and uninephrectomized (sham) rats served as controls.
The rise in systolic blood pressure in the perindopril-treated and losartan-treated rats was not significantly different from that in the untreated 1-K, 1C group throughout the treatment period. At 4 weeks after surgery the heart weight:body weight ratios of the untreated 1-K, 1C and losartan-treated 1-K, 1C groups were significantly greater than for sham-operated normotensive rats and hypertensive perindopril-treated rats. The total number of smooth muscle cells in the thoracic aortae of the 1-K, 1C untreated, losartan-treated 1-K, 1C and sham groups were similar. However, after treatment the aortae of the perindopril-treated group contained significantly fewer smooth muscle cells. The medial cross-sectional wall area and wall: lumen ratio were similar in the 1-K, 1C untreated and perindopril-treated 1-K, 1C groups.
These results suggest that Ang II, via its effects on cardiac and vascular AT1 receptors, does not contribute to the development of cardiovascular hypertrophy in the 1-K, 1C rat. Attenuation of cardiac and vascular growth after ACE inhibition appears to be mediated by mechanisms independent of the actions of the renin-angiotensin system.
研究血管紧张素II（Ang II）在戈德布拉特单肾单夹（1-K，1C）肾性高血压大鼠心血管肥厚中的作用。
六周龄的Wistar-Kyoto（WKY）大鼠接受单侧肾切除术和左肾动脉夹闭术。术后，大鼠用血管紧张素转换酶（ACE）抑制剂培哚普利或Ang II 1型（AT1）受体拮抗剂氯沙坦治疗4周。未治疗的1-K，1C大鼠和单侧肾切除（假手术）大鼠作为对照。
在整个治疗期间，培哚普利治疗组和氯沙坦治疗组大鼠收缩压的升高与未治疗的1-K，1C组相比无显著差异。术后4周，未治疗的1-K，1C组和氯沙坦治疗的1-K，1C组的心脏重量与体重之比显著高于假手术的正常血压大鼠和高血压培哚普利治疗组。1-K，1C未治疗组、氯沙坦治疗的1-K，1C组和假手术组胸主动脉平滑肌细胞总数相似。然而，治疗后培哚普利治疗组主动脉中的平滑肌细胞明显减少。1-K，1C未治疗组和培哚普利治疗的1-K，1C组的中膜横截面积和壁腔比相似。
这些结果表明，Ang II通过其对心脏和血管AT1受体的作用，对1-K，1C大鼠心血管肥厚的发展没有贡献。ACE抑制后心脏和血管生长的减弱似乎是由独立于肾素-血管紧张素系统作用的机制介导的。
