The ventrolateral medulla. A new site of action of the renin-angiotensin system.
The ventrolateral medulla. A new site of action of the renin-angiotensin system.
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延髓腹外侧。
DOI：
10.1161/01.hyp.11.2_pt_2.i163
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发表时间：
1988
期刊：
影响因子：
--
通讯作者：
Ferrario,CM
中科院分区：
文献类型：
--
作者：
Andreatta,SH;Averill,DB;Santos,RA;Ferrario,CM
高亲和力结合位点的血管紧张素II（Ang II）在腹外侧髓质表明，血管紧张素II可能会在细胞群，是已知的调节血压。这一假设进行了研究，局部应用血管紧张素I（Ang I），血管紧张素II，血管紧张素II拮抗剂[Sar 1，Thr 8]血管紧张素II，和血管紧张素I转化酶抑制剂MK 422腹侧延髓表面的一个限制性区域称为甘氨酸敏感区。血管紧张素I（100 pmol）和血管紧张素II（100 pmol）均使血压显著升高（p <0.01）（分别为+20 +/- 4和+31 +/- 5 mm Hg），但心率无变化。此外，血压升高峰值与Ang II之间的关系呈剂量依赖性。[Sar 1，Thr 8]Ang II（13 nmol）阻断内源性Ang II可显著降低基线血压（-8 +/- 1 mm Hg; p <0.001）。同样，局部应用MK 422可阻止Ang I的升压作用。两者合计，这些实验表明，至少有一些成分的肾素-血管紧张素系统存在于腹外侧髓质，他们可能会调节血管流出。
High-affinity binding sites for angiotensin II (Ang II) in the ventrolateral medulla suggest that Ang II may act at cell groups that are known to modulate blood pressure. This hypothesis was investigated by the topical application of angiotensin I (Ang I), Ang II, the Ang II antagonist [Sar1, Thr8]Ang II, and the Ang I converting enzyme inhibitor MK 422 to a restricted region of the ventral medullary surface known as the glycine-sensitive area. Both Ang I (100 pmol) and Ang II (100 pmol) produced significant (p less than 0.01) increases in blood pressure (+20 +/- 4 and +31 +/- 5 mm Hg, respectively) that were associated with no change in heart rate. Furthermore, the relationship between the peak increases in blood pressure and Ang II was dose-dependent. Blockade of endogenous Ang II by [Sar1, Thr8]Ang II (13 nmol) produced a significant decrease in baseline blood pressure (-8 +/- 1 mm Hg; p less than 0.001). Similarly, topical application of MK 422 prevented the pressor effect of Ang I. Taken together, these experiments indicate that at least some components of the renin-angiotensin system exist in the ventrolateral medulla and they may modulate vasomotor outflow.