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
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.