TY - JOUR
T1 - Endothelial dysfunction in resistance arteries is related to high blood pressure and circulating low density lipoproteins in previously treated hypertension
AU - Olsen, Michael Hecht
AU - Wachtell, Kristian
AU - Aalkjaer, Christian
AU - Devereux, Richard B.
AU - Dige-Petersen, Harriet
AU - Ibsen, Hans
PY - 2001/9/27
Y1 - 2001/9/27
N2 - Background: Peripheral endothelial dysfunction has been demonstrated in hypertension. However, its relationship to blood pressure (BP) load, vascular structure, and metabolic disturbances in patients with long-standing, previously treated hypertension is unclear. Methods: A total of 41 patients with stage I to III essential hypertension and electrocardiographic left ventricular hypertrophy were studied. After 2 to 3 weeks of placebo treatment we measured nitroprusside-induced relaxation (NIR), acetylcholine-induced relaxation (AIR), and media:lumen ratio in isolated, subcutaneous resistance arteries by myography, as well as 24-h ambulatory BP, and serum lipids. Results: Maximal AIR correlated negatively with median 24-h diastolic BP (r = -0.42, P = .01), and sensitivity to AIR correlated negatively with serum low density lipoprotein (LDL) (r = -0.36, P < .05). In multiple regression analyses, sensitivity to AIR correlated negatively with serum LDL (β = -0.33) independently of maximal NIR (β = 0.41) (adjusted R2 = 0.26, P < .01). Maximal acetylcholine-induced relaxation correlated negatively with median 24-h diastolic BP (β = -0.38) independently of maximal NIR (β = 0.45) (adjusted R2 = 0.32, P < .001). Acetylcholine-induced relaxation was not significantly related to diabetes or to media:lumen ratio (r = -0.26, NS). Conclusions: High diastolic BP and high serum LDL were associated with impaired maximal AIR and reduced sensitivity to AIR, respectively, independently of smooth muscle cell responsiveness to nitroprusside. This indicated decreasing endothelial function in small resistance arteries with increasing BP and increasing LDL in hypertension. Endothelial function was not significantly related to vascular structure of the resistance arteries or to diabetes in these patients with long-standing hypertension.
AB - Background: Peripheral endothelial dysfunction has been demonstrated in hypertension. However, its relationship to blood pressure (BP) load, vascular structure, and metabolic disturbances in patients with long-standing, previously treated hypertension is unclear. Methods: A total of 41 patients with stage I to III essential hypertension and electrocardiographic left ventricular hypertrophy were studied. After 2 to 3 weeks of placebo treatment we measured nitroprusside-induced relaxation (NIR), acetylcholine-induced relaxation (AIR), and media:lumen ratio in isolated, subcutaneous resistance arteries by myography, as well as 24-h ambulatory BP, and serum lipids. Results: Maximal AIR correlated negatively with median 24-h diastolic BP (r = -0.42, P = .01), and sensitivity to AIR correlated negatively with serum low density lipoprotein (LDL) (r = -0.36, P < .05). In multiple regression analyses, sensitivity to AIR correlated negatively with serum LDL (β = -0.33) independently of maximal NIR (β = 0.41) (adjusted R2 = 0.26, P < .01). Maximal acetylcholine-induced relaxation correlated negatively with median 24-h diastolic BP (β = -0.38) independently of maximal NIR (β = 0.45) (adjusted R2 = 0.32, P < .001). Acetylcholine-induced relaxation was not significantly related to diabetes or to media:lumen ratio (r = -0.26, NS). Conclusions: High diastolic BP and high serum LDL were associated with impaired maximal AIR and reduced sensitivity to AIR, respectively, independently of smooth muscle cell responsiveness to nitroprusside. This indicated decreasing endothelial function in small resistance arteries with increasing BP and increasing LDL in hypertension. Endothelial function was not significantly related to vascular structure of the resistance arteries or to diabetes in these patients with long-standing hypertension.
KW - Endothelial function
KW - Hypertension
KW - Lipids
KW - Vascular structure
UR - http://www.scopus.com/inward/record.url?scp=0034832451&partnerID=8YFLogxK
U2 - 10.1016/S0895-7061(01)02148-3
DO - 10.1016/S0895-7061(01)02148-3
M3 - Article
C2 - 11587150
AN - SCOPUS:0034832451
VL - 14
SP - 861
EP - 867
JO - American Journal of Hypertension
JF - American Journal of Hypertension
SN - 0895-7061
IS - 9 I
ER -