Transient hypertension directly impairs endothelium-dependent vasodilationof the human microvasculature

Citation
Oa. Paniagua et al., Transient hypertension directly impairs endothelium-dependent vasodilationof the human microvasculature, HYPERTENSIO, 36(6), 2000, pp. 941-944
Citations number
17
Language
INGLESE
art.tipo
Article
Categorie Soggetti
Cardiovascular & Respiratory Systems","Cardiovascular & Hematology Research
Journal title
HYPERTENSION
ISSN journal
0194-911X → ACNP
Volume
36
Issue
6
Year of publication
2000
Pages
941 - 944
Database
ISI
SICI code
0194-911X(200012)36:6<941:THDIEV>2.0.ZU;2-4
Abstract
Hypertension is associated with decreased endothelium-dependent vasodilatio n. However, whether endothelial dysfunction is a cause or a consequence of elevated blood pressure is unknown. Therefore, to determine whether hyperte nsion can directly induce endothelial dysfunction, we investigated the effe ct of increases in intra-arterial pressure on endothelium-dependent vasodil ation of the human microvasculature. Small arteries (internal diameter 202/-75 mum) were isolated from gluteal fat biopsies in 12 healthy normotensiv e subjects (8 men and 4 women; age, 46+/-10 years). Arteries were cannulate d and perfused in chambers oxygenated at 37 degreesC. Endothelium-dependent and -independent responses to acetylcholine (Ach; 10(-9) to 10(-4) mol/L) and sodium nitroprusside (SNP; 10(-9) to 10(-4) mol/L), respectively, were obtained after incubating the vessel with incremental intravascular pressur es of 50, 80, and 120 mm Hg for 60 minutes each. The response to Ach was al so obtained in different arteries after 3 consecutive incubation periods at 50 mm Hg. Arterial internal diameter was measured directly from amplified digital images. A significant reduction in the vasodilator response to Ach was observed with increases in intravascular pressure (mean vasodilation, 6 2%, 49%, and 26% at 50, 80, and 120 mm Hg, respectively; P<0.001). In contr ast, the response to SNP showed a nonsignificant trend toward greater vasod ilation with increases in pressure (mean vasodilation, 40%, 52%, and 57% at 50, 80, and 120 mm Hg, respectively; P=0.10). There was no difference in t he consecutive dose-response curves to Ach obtained at the same intravascul ar pressure (mean vasodilation: 48%, 46%, and 49%; P=0.61). Transient incre ases in intravascular pressure significantly depress endothelium-dependent vasodilation in human resistance arteries. These findings suggest that elev ated blood pressure per se may cause endothelial dysfunction in humans and have implications for the pathophysiology of endothelial dysfunction in hyp ertension.