Black M J, Campbell J H, Campbell G R
Baker Medical Research Institute, Melbourne, Victoria, Australia.
Am J Cardiol. 1993 Jun 24;71(17):17E-21E. doi: 10.1016/0002-9149(93)90947-b.
The aim was to determine whether cardiovascular hypertrophy in primary hypertension in the spontaneously hypertensive rat (SHR) is induced by increased levels of angiotensin II or by increased blood pressure. SHR were treated from 7 to 15 weeks of age with perindopril to block the in vivo production of A II and concomitantly infused with either a pressor dose of norepinephrine or angiotensin II. At the end of the treatment period, there was no significant difference in the systolic blood pressure in the norepinephrine or angiotensin II-treated groups (201 +/- 9 and 208 +/- 8 mm Hg, respectively). However, there was a significant increase (p < 0.01) in left ventricle-plus-septum/body weight ratio in angiotensin II compared with norepinephrine-infused SHR (3.72 +/- 0.25 and 2.34 +/- 0.04 mg/g, respectively) and in aortic medial cross-sectional area (0.55 +/- 0.05 and 0.38 +/- 0.01 mm2, respectively). Using an unbiased optical dissector/fractionator technique, the number of smooth muscle cells in the descending thoracic aorta of the angiotensin II-infused SHR was not different from norepinephrine-infused rats (5.02 +/- 0.30 x 10(6) and 4.71 +/- 0.42 x 10(6) cells, respectively), and no difference in size of enzyme-isolated cells was observed (mode: 1,326 +/- 127 microns 3 compared with 1,186 +/- 82 microns 3). The results indicate that angiotensin II directly stimulates cardiac and aortic hypertrophy through a mechanism unrelated to its effect on blood pressure. The aortic hypertrophy is not due to an increase in smooth muscle cell size or number and thus must be related to an increase in the extracellular compartment.
目的是确定自发性高血压大鼠（SHR）原发性高血压中的心血管肥大是由血管紧张素II水平升高还是血压升高引起的。在7至15周龄时，用培哚普利治疗SHR以阻断体内A II的产生，并同时输注升压剂量的去甲肾上腺素或血管紧张素II。在治疗期结束时，去甲肾上腺素或血管紧张素II治疗组的收缩压无显著差异（分别为201±9和208±8 mmHg）。然而，与输注去甲肾上腺素的SHR相比，输注血管紧张素II的SHR的左心室加室间隔/体重比显著增加（p <0.01）（分别为3.72±0.25和2.34±0.04 mg/g），主动脉中膜横截面积也显著增加（分别为0.55±0.05和0.38±0.01 mm2）。使用无偏倚光学分割器/分馏器技术，输注血管紧张素II的SHR的降主动脉平滑肌细胞数量与输注去甲肾上腺素的大鼠无差异（分别为5.02±0.30×10(6)和4.71±0.42×10(6)个细胞），并且未观察到酶分离细胞大小的差异（模式：1,326±127微米3与1,186±82微米3）。结果表明，血管紧张素II通过与其对血压的影响无关的机制直接刺激心脏和主动脉肥大。主动脉肥大不是由于平滑肌细胞大小或数量的增加，因此必须与细胞外间隙的增加有关。
