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氯沙坦阻断血管紧张素受体可减弱盐负荷高血压受试者对手握力收缩的升压反应并增强利钠作用:一项针对尼日利亚成年人的准实验研究。

Angiotensin receptor blockade with Losartan attenuates pressor response to handgrip contraction and enhances natriuresis in salt loaded hypertensive subjects: a quasi-experimental study among Nigerian adults.

作者信息

Agbaraolorunpo Francis Muyiwa, Sofola Olusoga Adekunle, Anigbogu Chikodi Nnanyelu, Azinge Elaine Chinyelu

机构信息

Department of Physiology, College of Medicine, University of Lagos, Lagos, Nigeria.

Department of Clinical Pathology, College of Medicine, University of Lagos, Lagos, Nigeria.

出版信息

Pan Afr Med J. 2019 Dec 9;34:188. doi: 10.11604/pamj.2019.34.188.18317. eCollection 2019.

Abstract

INTRODUCTION

Sympathetic and Renin-Angiotensin-Aldosterone systems play crucial roles in blood pressure response to increased salt intake. This study investigated the effects of angiotensin receptor blocker (ARB) and sympathetic excitation on the responses of blood pressure (BP) and peripheral vascular resistance (PVR) in salt loaded normotensive (NT) and hypertensive (HT) Nigerian subjects.

METHODS

16 NT and 14 HT participants, that were age-matched [39.9 ± 1.3 vs 44.1±2.1yrs (P= 0.10)], underwent 5 days each of oral administration of 200mmol NaCl, and 200mmol NaCl + 50mg Losartan, preceded by a baseline control condition. BP and PVR responses to 30% Maximum Voluntary Contraction (MVC) of handgrip (HG) for one minute were determined at baseline, after salt load and after salt + Losartan. Data were presented as Mean ± SEM, and analyzed with two-way ANOVA and paired t-test, with P<0.05 accepted as significant.

RESULTS

BP and PVR were significantly increased by HG at baseline, after salt load and after salt + Losartan in NT and HT. Salt load augmented the HG-induced SBP (P=0.04) and MABP responses (P=0.02) in HT. While Losartan attenuated the HG- induced Systolic Blood Pressure (SBP) SBP response (P=0.007) and DBP response (P=0.003) in HT and NT respectively after salt + Losartan. HG-induced PVR response was significantly accentuated after salt load in HT (P=0.005), but it was not significant in NT (P=0.38).

CONCLUSION

The implication of our finding is that angiotensin II receptor blockade possibly attenuates salt-induced sympathetic nerve excitation in black hypertensive patients.

摘要

引言

交感神经系统和肾素-血管紧张素-醛固酮系统在血压对盐摄入增加的反应中起着关键作用。本研究调查了血管紧张素受体阻滞剂(ARB)和交感神经兴奋对盐负荷正常血压(NT)和高血压(HT)尼日利亚受试者的血压(BP)和外周血管阻力(PVR)反应的影响。

方法

16名NT参与者和14名HT参与者年龄匹配[39.9±1.3岁对44.1±2.1岁(P = 0.10)],在基线对照条件之前,分别接受5天每天口服200mmol氯化钠和200mmol氯化钠+50mg氯沙坦的治疗。在基线、盐负荷后和盐+氯沙坦后,测定对握力(HG)进行1分钟的30%最大自主收缩(MVC)时的血压和外周血管阻力反应。数据以平均值±标准误表示,并用双向方差分析和配对t检验进行分析,P<0.05被认为具有统计学意义。

结果

在NT和HT中,基线时、盐负荷后以及盐+氯沙坦后,HG均显著升高血压和外周血管阻力。盐负荷增强了HT中HG诱导的收缩压(SBP)(P = 0.04)和平均动脉压反应(P = 0.02)。而氯沙坦在盐+氯沙坦后分别减弱了HT和NT中HG诱导的收缩压(SBP)反应(P = 0.007)和舒张压反应(P = 0.003)。盐负荷后,HT中HG诱导的外周血管阻力反应显著增强(P = 0.005),但在NT中不显著(P = 0.38)。

结论

我们研究结果的意义在于,血管紧张素II受体阻断可能减弱黑人高血压患者盐诱导的交感神经兴奋。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/008c/7060958/37607da06370/PAMJ-34-188-g001.jpg

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