Differential effects of antihypertensive drug therapy on vascular smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in the spontaneously hypertensive rat.
Differential effects of antihypertensive drug therapy on vascular smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in the spontaneously hypertensive rat.
复制标题
抗高血压药物治疗对自发性高血压大鼠血管平滑肌细胞肥大、超倍体和增生的不同影响。
DOI：
10.1161/01.res.56.4.525
复制
发表时间：
1985
影响因子：
20.1
通讯作者：
Owens,GK
中科院分区：
文献类型：
--
作者：
Owens,GK
本报告扩展了我们以前的研究，平滑肌细胞肥大，超倍体，增生的5个月大的自发性高血压和Wistar-Kyoto大鼠，包括3个月和7个月大的大鼠的分析，并探讨了抗高血压药物治疗的影响，血管平滑肌在血管平滑肌的自发性高血压vs. Wistar-Kyoto大鼠动脉瘤的加速生长。给药组大鼠在3 - 5月龄或5 - 7月龄时，在其饮用水中加入利血平、肼苯哒嗪和氯噻嗪。药物治疗降低自发性高血压大鼠的血压值等于或低于两个年龄治疗组的Wistar-Kyoto大鼠。通过主动脉平滑肌含量的形态学分析、多倍体平滑肌细胞频率的流式细胞术和显微光密度测量、主动脉中膜平滑肌细胞数量的生物化学估计和单个平滑肌细胞蛋白含量的显微光密度测量来评价平滑肌生长。获得了以下结果。与Wistar-Kyoto大鼠相比，3个月自发性高血压大鼠的主动脉中膜平滑肌含量没有显著增加，表明主动脉平滑肌肥大发生在3个月后以及血压升高后。在5个月大的自发性高血压和Wistar-Kyoto大鼠中，中膜平滑肌肥大可以解释为细胞肥大而不增生;相反，7个月大的自发性高血压大鼠中膜肥大涉及细胞肥大和增生。抗高血压治疗通过细胞肥大和超倍体阻止了自发性高血压大鼠中发生的血管平滑肌加速生长，但不能阻止5 - 7月龄自发性高血压大鼠中平滑肌细胞数量的增加。此外，它对3 - 5月龄自发性高血压大鼠和Wistar-Kyoto大鼠主动脉中膜平滑肌细胞数量的平行增加没有影响。尽管药物治疗阻止了自发性高血压大鼠平滑肌细胞多倍体的加速发展，但在任何情况下（自发性高血压或Wistar-Kyoto大鼠），药物治疗都没有逆转药物治疗开始时存在的倍性变化，尽管药物治疗确实导致了每种倍性类别平滑肌细胞的细胞萎缩。（400字处截断摘要）
The present report extends our previous studies of smooth muscle cell hypertrophy, hyperploidy, and hyperplasia in the 5-month-old spontaneously hypertensive and Wistar-Kyoto rats to include analyses of 3- and 7-month-old rats and explores the effects of antihypertensive drug treatment on the accelerated growth of vascular smooth muscle in aortas of spontaneously hypertensive vs. Wistar-Kyoto rats. Drug-treated rats were administered a combination of reserpine, hydralazine, and chlorathiazide in their drinking water, either between 3 and 5 months or between 5 and 7 months of age. Drug treatment decreased the blood pressure of spontaneously hypertensive rats to values at or below those of Wistar-Kyoto rats for both age-treatment groups. Smooth muscle growth was evaluated by morphometric analyses of aortic smooth muscle content, flow cytometric and microdensitometric measurements of the frequency of polyploid smooth muscle cells, biochemical estimates of aortic medial smooth muscle cell number, and microdensitometric measurements of individual smooth muscle cell protein content. The following results were obtained. Aortic medial smooth muscle content was not significantly increased in 3-month spontaneously hypertensive compared to Wistar-Kyoto rats, indicating that aortic smooth muscle hypertrophy occurred post-3 months, as well as after blood pressure was elevated. In 5-month-old spontaneously hypertensive and Wistar-Kyoto rats, medial smooth muscle hypertrophy could be accounted for by cellular hypertrophy without hyperplasia; in contrast, medial hypertrophy in 7-month-old spontaneously hypertensive rats involved both cellular hypertrophy and hyperplasia. Antihypertensive treatment prevented the accelerated growth of vascular smooth muscle that occurred in spontaneously hypertensive rats via cellular hypertrophy and hyperploidy, but it did not prevent an increase in smooth muscle cell number in spontaneously hypertensive rats between 5 and 7 months of age. Furthermore, it had no effect on the parallel increases in aortic medial smooth muscle cell number that occurred in both spontaneously hypertensive and Wistar-Kyoto rats between 3 and 5 months of age. Whereas drug treatment prevented accelerated development of smooth muscle cell polyploidism in spontaneously hypertensive rats, in no case (spontaneously hypertensive or Wistar-Kyoto rats) did it reverse changes in ploidy that existed at the time of initiation of drug treatment, although it did cause cellular atrophy in smooth muscle cells of each ploidy class.(ABSTRACT TRUNCATED AT 400 WORDS)