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大鼠动脉平滑肌细胞增生与肾性高血压的发生及逆转相关。

Hyperplasia of rat arteries smooth muscle cells associated with development and reversal of renal hypertension.

作者信息

Rorive G L, Carlier P J, Foidart J M

出版信息

Clin Sci (Lond). 1980 Dec;59 Suppl 6:335s-338s. doi: 10.1042/cs059335s.

Abstract
  1. Renal hypertension produces a marked and rapidly detectable hypertrophy of the rat aorta, due to smooth muscle cell hyperplasia and connective tissue deposition. 2. As we described previously for collagen synthesis, cell hyperplasia is a very early event which reaches a maximum at a time when the blood pressure is far from its highest level, and thereafter progressively decreases. 3. Reserpine prevents the vascular wall changes on the arterial as well as the venous side of the circulation. On the other hand, captopril although effective in preventing the blood pressure rise does not suppress the hyperplastic response. 4. The arterial hypertensive disease appears to be reversible, when renal ischaemia is corrected. The smooth muscle cell hyperplasia is, however, only partly and slowly reversible. 5. These data suggest that blood pressure is not the only determinant of the vascular wall response, and that the effect of a drug on the blood pressure does nt necessarily predict the vascular wall response.
摘要
  1. 肾性高血压会导致大鼠主动脉显著且能迅速检测到的肥大,这是由于平滑肌细胞增生和结缔组织沉积所致。2. 正如我们之前所描述的胶原蛋白合成情况,细胞增生是一个非常早期的事件,在血压远未达到最高水平时达到最大值,此后逐渐下降。3. 利血平可防止循环中动脉和静脉侧的血管壁变化。另一方面,卡托普利虽然能有效防止血压升高,但并不能抑制增生反应。4. 当肾缺血得到纠正时,动脉高血压疾病似乎是可逆的。然而,平滑肌细胞增生只是部分且缓慢可逆。5. 这些数据表明,血压并非血管壁反应的唯一决定因素,而且药物对血压的影响不一定能预测血管壁反应。

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