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L-/N型钙通道阻滞剂对高血压患者血管紧张素II-肾素反馈的影响

Effects of L-/N-Type Calcium Channel Blockers on Angiotensin II-Renin Feedback in Hypertensive Patients.

作者信息

Kawabata Yutaka, Soeki Takeshi, Ito Hiroyuki, Matsuura Tomomi, Kusunose Kenya, Ise Takayuki, Yamaguchi Koji, Tobiume Takeshi, Yagi Shusuke, Fukuda Daiju, Yamada Hirotsugu, Wakatsuki Tetsuzo, Kitani Mitsuhiro, Kawano Kazuhiro, Taketani Yoshio, Sata Masataka

机构信息

Department of Cardiovascular Medicine, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.

Department of Cardio-Diabetes Medicine, Tokushima University Graduate School of Biomedical Sciences, Tokushima, Japan.

出版信息

Int J Hypertens. 2020 Dec 22;2020:6653851. doi: 10.1155/2020/6653851. eCollection 2020.

DOI:10.1155/2020/6653851
PMID:33489354
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7803135/
Abstract

OBJECTIVES

Cilnidipine, an L-/N-type calcium channel blocker (CCB), has unique organ-protective properties due to suppression of hyperactivity in the sympathetic nervous system and renin-angiotensin system (RAS). In this study, we hypothesized that cilnidipine might exert a renoprotective effect by suppressing the RAS.

METHODS

A total of 25 hypertensive patients receiving a RAS inhibitor were randomly assigned to a cilnidipine ( = 12) or amlodipine ( = 13) group. The effects of cilnidipine on proteinuria and angiotensin II-renin feedback were assessed.

RESULTS

After 6 months of treatment, both systolic and diastolic blood pressures were significantly reduced to a similar extent in both groups. The urine albumin-to-creatinine ratio was significantly lower in the cilnidipine group ( < 0.05) than in the amlodipine group. Amlodipine increased plasma angiotensin I and angiotensin II levels ( < 0.05), whereas cilnidipine did not. Interestingly, the cilnidipine group had a higher ratio of angiotensin-(1-7) (Ang-(1-7)) to angiotensin II in plasma than the amlodipine group ( < 0.05).

CONCLUSIONS

The L-/N-type CCB cilnidipine, but not amlodipine, decreased urinary albumin excretion in hypertensive patients. Cilnidipine also increased the ratio of Ang-(1-7) to angiotensin II in plasma, which might be one factor underlying its beneficial effects.

摘要

目的

西尼地平是一种L-/N型钙通道阻滞剂（CCB），由于其对交感神经系统和肾素-血管紧张素系统（RAS）过度激活的抑制作用而具有独特的器官保护特性。在本研究中，我们假设西尼地平可能通过抑制RAS发挥肾脏保护作用。

方法

将25例接受RAS抑制剂治疗的高血压患者随机分为西尼地平组（n = 12）和氨氯地平组（n = 13）。评估西尼地平对蛋白尿和血管紧张素II-肾素反馈的影响。

结果

治疗6个月后，两组的收缩压和舒张压均显著降低，且降低程度相似。西尼地平组的尿白蛋白与肌酐比值显著低于氨氯地平组（P < 0.05）。氨氯地平使血浆血管紧张素I和血管紧张素II水平升高（P < 0.05），而西尼地平则没有。有趣的是，西尼地平组血浆中血管紧张素-(1-7)（Ang-(1-7)）与血管紧张素II的比值高于氨氯地平组（P < 0.05）。

结论

L-/N型CCB西尼地平而非氨氯地平可降低高血压患者的尿白蛋白排泄。西尼地平还增加了血浆中Ang-(1-7)与血管紧张素II的比值，这可能是其有益作用的一个潜在因素。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/cdf3cc8ff0b4/ijhy2020-6653851.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/d9d3c52d2d36/ijhy2020-6653851.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/7b0ed65edb1a/ijhy2020-6653851.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/5d2301dca869/ijhy2020-6653851.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/b464bf3c770e/ijhy2020-6653851.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/ce880f3366bd/ijhy2020-6653851.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/ad138f633878/ijhy2020-6653851.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/cdf3cc8ff0b4/ijhy2020-6653851.007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/d9d3c52d2d36/ijhy2020-6653851.001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/7b0ed65edb1a/ijhy2020-6653851.002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/5d2301dca869/ijhy2020-6653851.003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/b464bf3c770e/ijhy2020-6653851.004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/ce880f3366bd/ijhy2020-6653851.005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/ad138f633878/ijhy2020-6653851.006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/59f0/7803135/cdf3cc8ff0b4/ijhy2020-6653851.007.jpg

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ACE2: angiotensin II/angiotensin-(1-7) balance in cardiac and renal injury.
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