有中风家族史的高血压患者一氧化氮释放受损。

Nitric oxide release is impaired in hypertensive individuals with familial history of stroke.

作者信息

Cosentino Francesco, Francia Pietro, Musumeci Beatrice, De Siati Luca, Rao Maria Assunta, De Luca Nicola, Balla Cristina, De Sensi Francesco, Volpe Massimo

机构信息

Division of Cardiology, 2(nd) Faculty of Medicine, University La Sapienza, Rome, Italy.

出版信息

Am J Hypertens. 2006 Dec;19(12):1213-6. doi: 10.1016/j.amjhyper.2006.06.002.

DOI:10.1016/j.amjhyper.2006.06.002

PMID:17161765

Abstract

BACKGROUND

A genetic origin of cerebrovascular accidents has long been suspected on the basis of epidemiologic evidence and familial aggregation. Nevertheless, the final phenotype is largely influenced by concomitant risk factors. We aimed to investigate whether impairment of endothelium-dependent vasodilation can be used as an informative intermediate vascular phenotype in hypertensive patients with familial history of stroke.

METHODS

Fourteen hypertensive individuals, seven with familial history of stroke (FH+), seven without familial history of stroke (FH-), and six normotensive volunteers (C) were included in the study. High-resolution ultrasound and Doppler were used to measure radial artery diameter and blood flow at rest, during reactive hyperemia, and after intra-arterial infusion of N(G)-monomethyl-l-arginine (L-NMMA) to inhibit NO synthase.

RESULTS

Basal blood flow and diameter were comparable in all groups. Flow-mediated dilation was impaired in FH+ (3.2% +/- 2%), compared with FH- (9.6% +/- 1%; P = . 01) and C (15.9% +/- 3%; P = . 001). The L-NMMA decreased basal flow in FH- (16.0 +/- 2 v 13.8 +/- 1 mL/min; P = . 04), and C (23.3 +/- 2 v 16.5 +/- 2 mL/min, P = .003) but did not exert any significant effect in FH+ subjects (16.4 +/- 3 v 15.8 +/- 2 mL/min, P = .77).

CONCLUSIONS

These findings demonstrate that NO bioavailability is reduced in hypertensive subjects with familial history of stroke. Such a phenotype may represent an early marker of susceptibility to cerebrovascular events in this population.

摘要

背景

长期以来，基于流行病学证据和家族聚集现象，人们一直怀疑脑血管意外存在遗传起源。然而，最终的表型在很大程度上受伴随的危险因素影响。我们旨在研究内皮依赖性血管舒张功能障碍是否可作为有中风家族史的高血压患者一种有用的中间血管表型。

方法

本研究纳入了14名高血压患者，其中7名有中风家族史（FH+），7名无中风家族史（FH-），以及6名血压正常的志愿者（C）。采用高分辨率超声和多普勒技术测量静息状态下、反应性充血期间以及动脉内注入N（G）-单甲基-L-精氨酸（L-NMMA）以抑制一氧化氮合酶后桡动脉直径和血流情况。

结果

所有组的基础血流和直径相当。与FH-组（9.6%±1%）和C组（15.9%±3%）相比，FH+组的血流介导的血管舒张功能受损（3.2%±2%；P = 0.01；P = 0.001）。L-NMMA使FH-组（16.0±2对13.8±1 mL/分钟；P = 0.04）和C组（23.3±2对16.5±2 mL/分钟，P = 0.003）的基础血流降低，但对FH+组受试者无显著影响（16.4±3对15.8±2 mL/分钟，P = 0.77）。