Nitric Oxide Release Is Impaired in Hypertensive Individuals With Familial History of Stroke

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

Research output: Contribution to journalArticle

7 Citations (Scopus)

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 NG-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.

Original languageEnglish
Pages (from-to)1213-1216
Number of pages4
JournalAmerican Journal of Hypertension
Volume19
Issue number12
DOIs
Publication statusPublished - Dec 2006

Fingerprint

Nitric Oxide
Stroke
omega-N-Methylarginine
Phenotype
Doppler Ultrasonography
Intra Arterial Infusions
Radial Artery
Hyperemia
Vasodilation
Nitric Oxide Synthase
Biological Availability
Endothelium
Blood Vessels
Arginine
Dilatation
Volunteers
Population

Keywords

  • endothelial dysfunction
  • flow-dependent dilation
  • Hypertension
  • nitric oxide
  • stroke

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

Nitric Oxide Release Is Impaired in Hypertensive Individuals With Familial History of Stroke. / Cosentino, Francesco; Francia, Pietro; Musumeci, Beatrice; De Siati, Luca; Rao, Maria Assunta; De Luca, Nicola; Balla, Cristina; De Sensi, Francesco; Volpe, Massimo.

In: American Journal of Hypertension, Vol. 19, No. 12, 12.2006, p. 1213-1216.

Research output: Contribution to journalArticle

Cosentino, F, Francia, P, Musumeci, B, De Siati, L, Rao, MA, De Luca, N, Balla, C, De Sensi, F & Volpe, M 2006, 'Nitric Oxide Release Is Impaired in Hypertensive Individuals With Familial History of Stroke', American Journal of Hypertension, vol. 19, no. 12, pp. 1213-1216. https://doi.org/10.1016/j.amjhyper.2006.06.002
Cosentino, Francesco ; Francia, Pietro ; Musumeci, Beatrice ; De Siati, Luca ; Rao, Maria Assunta ; De Luca, Nicola ; Balla, Cristina ; De Sensi, Francesco ; Volpe, Massimo. / Nitric Oxide Release Is Impaired in Hypertensive Individuals With Familial History of Stroke. In: American Journal of Hypertension. 2006 ; Vol. 19, No. 12. pp. 1213-1216.
@article{41693d515031422090e5af40bd0a0bdd,
title = "Nitric Oxide Release Is Impaired in Hypertensive Individuals With Familial History of Stroke",
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 NG-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.",
keywords = "endothelial dysfunction, flow-dependent dilation, Hypertension, nitric oxide, stroke",
author = "Francesco Cosentino and Pietro Francia and Beatrice Musumeci and {De Siati}, Luca and Rao, {Maria Assunta} and {De Luca}, Nicola and Cristina Balla and {De Sensi}, Francesco and Massimo Volpe",
year = "2006",
month = "12",
doi = "10.1016/j.amjhyper.2006.06.002",
language = "English",
volume = "19",
pages = "1213--1216",
journal = "American Journal of Hypertension",
issn = "0895-7061",
publisher = "Oxford University Press",
number = "12",

}

TY - JOUR

T1 - Nitric Oxide Release Is Impaired in Hypertensive Individuals With Familial History of Stroke

AU - Cosentino, Francesco

AU - Francia, Pietro

AU - Musumeci, Beatrice

AU - De Siati, Luca

AU - Rao, Maria Assunta

AU - De Luca, Nicola

AU - Balla, Cristina

AU - De Sensi, Francesco

AU - Volpe, Massimo

PY - 2006/12

Y1 - 2006/12

N2 - 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 NG-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.

AB - 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 NG-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.

KW - endothelial dysfunction

KW - flow-dependent dilation

KW - Hypertension

KW - nitric oxide

KW - stroke

UR - http://www.scopus.com/inward/record.url?scp=33845186131&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=33845186131&partnerID=8YFLogxK

U2 - 10.1016/j.amjhyper.2006.06.002

DO - 10.1016/j.amjhyper.2006.06.002

M3 - Article

VL - 19

SP - 1213

EP - 1216

JO - American Journal of Hypertension

JF - American Journal of Hypertension

SN - 0895-7061

IS - 12

ER -