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 language | English |
|---|---|
| Pages (from-to) | 1213-1216 |
| Number of pages | 4 |
| Journal | American Journal of Hypertension |
| Volume | 19 |
| Issue number | 12 |
| DOIs | |
| Publication status | Published - Dec 2006 |
Fingerprint
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 journal › Article
}
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 -