Effect of cross-transplantation on normotensive and spontaneously hypertensive rat arterial muscle membrane.

Effect of cross-transplantation on normotensive and spontaneously hypertensive rat arterial muscle membrane.
复制标题

交叉移植对正常血压和自发性高血压大鼠动脉肌膜的影响。

DOI:
10.1161/01.hyp.3.5.534
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发表时间:
1981
期刊:
Hypertension (Dallas, Tex. : 1979)
影响因子:
--
通讯作者:
Hermsmeyer,K
Hermsmeyer,K
中科院分区:
--
文献类型:
--
作者:
Campbell,GR;Chamley-Campbell,J;Short,N;Robinson,RB;Hermsmeyer,K

文献摘要

相似文献

将动脉移植到大鼠的前眼房中8周用于检验神经体液环境在建立高血压中血管肌肉的改变的膜电位(在生电离子转运抑制期间可观察到)中是重要的假设。将12 ~ 16周龄自发性高血压大鼠(SHR)或遗传学匹配的正常血压大鼠(KNR)的尾动脉移植到对侧品系,动脉肌细胞的转运抑制膜电位(Em)与新鲜切取的供体动脉相比无变化。然而,当尾动脉从2周龄的动物移植到眼前房,动脉总是开发适当的Em宿主动物。换句话说,遗传上的KNR动脉在SHR宿主中发育了SHR动脉的Em;相反,遗传上的SHR动脉在KNR宿主中发育了KNR动脉的Em。这些结果表明:(1)SHR和KNR尾动脉Em的差异不是肌细胞本身固有的,(2)Em的变化在高血压形成前就已触发,而在高血压形成后不触发;尾动脉的Em改变与血压升高引起的动脉结构变化无关(因为KNR移植物不与宿主眼前房脉管系统串联连接,并且不受升高的血压的影响)。我们的结论是,动脉肌细胞到一定的年龄响应于一个外部因素,调节他们的EM和推测他们的血管加压剂的敏感性。
Transplantation of arteries into the anterior eye chamber of rats for 8 weeks was used to test the hypothesis that the neurohumoral environment is important in establishing the altered membrane potential (observable during electrogenic ion transport inhibition) of vascular muscle in hypertension. When caudal arteries from 12- to 16-week-old spontaneously hypertensive rats (SHR) or genetically matched Kyoto-Wistar normotensive rats (KNR) were transplanted into the opposite strain, there was no change in the transport inhibited membrane potential (Em) of the arterial muscle cells from that found in freshly excised donor arteries. However, when caudal arteries from 2-week-old animals were transplanted into the anterior eye chamber, the arteries always developed the appropriate Em for the host animal. In other words, a genetically KNR artery developed the Em of an SHR artery in an SHR host; conversely, a genetically SHR artery developed the Em of a KNR artery in the KNR host. These results provide evidence that: 1) the differences between th Em of caudal arteries from SHR and KNR are not inherent in those muscle cells; 2) the change in Em is triggered in young animals preceding development of hypertension, but not after hypertension is established; and 3) the Em alteration of the caudal artery is independent of structural changes that occur in the artery as a result of increased blood pressure (because KNR transplants were not connected in series with the host anterior eye chamber vasculature and subject to the elevated blood pressures). We conclude that the arterial muscle cells up to a certain age respond to an external factor that regulates their Em and presumably their sensitivity to vasopressor agents.