Endothelial function in subjects with isolated low HDL cholesterol: role of nitric oxide and circulating progenitor cells

Autor: Kazuaki Chayama, Hidekazu Umei, Junko Soga, Yasuki Kihara, Hidehiro Matsuoka, Yuichi Fujii, Ryo Sugano, Tsutomu Imaizumi, Yukihito Higashi
Rok vydání: 2010
Předmět:
Adult
Male
Vascular Endothelial Growth Factor A
medicine.medical_specialty
Endothelium
Physiology
Vasodilator Agents
Endocrinology
Diabetes and Metabolism

Biology
Nitric Oxide
Statistics
Nonparametric

Nitric oxide
Cohort Studies
Nitroglycerin
Young Adult
chemistry.chemical_compound
High-density lipoprotein
Reference Values
Risk Factors
Physiology (medical)
Internal medicine
medicine
Humans
Progenitor cell
Aged
Pravastatin
Aged
80 and over

Cholesterol
Anticholesteremic Agents
Stem Cells
Cholesterol
HDL

nutritional and metabolic diseases
Middle Aged
Vasodilation
Endocrinology
medicine.anatomical_structure
chemistry
Cardiovascular Diseases
Case-Control Studies
Circulatory system
Female
lipids (amino acids
peptides
and proteins)

Endothelium
Vascular

Hydroxymethylglutaryl-CoA Reductase Inhibitors
Lipoprotein
Blood vessel
Zdroj: American Journal of Physiology-Endocrinology and Metabolism. 298:E202-E209
ISSN: 1522-1555
0193-1849
Popis: Epidemiologic studies have shown that a low level of high-density lipoprotein (HDL) cholesterol is a risk factor for cardiovascular diseases. The purpose of this study was to determine the contribution of isolated low HDL cholesterol to endothelial function. Thirty-nine subjects with low HDL cholesterol who had no other cardiovascular risk factors were selected from the 5,417 participants from our population. We evaluated flow-mediated vasodilation (FMD) before and after 4 wk of treatment with the HMG-CoA reductase inhibitor pravastatin in 29 of the 39 subjects with isolated low HDL cholesterol. FMD was lower in the low-HDL-cholesterol group ( n = 29) than in the control group ( n = 29), whereas NTG-induced vasodilation was similar in the two groups. Pravastatin increased HDL cholesterol, urinary excretion of nitrite/nitrate, circulating levels of progenitor cells, and cell migration response to vascular endothelial growth factor in 15 subjects with low HDL cholesterol but not in 14 placebo control subjects. FMD increased in the pravastatin treatment group but not in the control group. NTG-induced vasodilation was similar before and after 4 wk of treatment in the two groups. Multiple regression analysis revealed that changes in HDL cholesterol, the number of progenitor cells, and migration of progenitor cells were independent predictors of augmentation of FMD with pravastatin. These findings suggest that low HDL cholesterol is an independent risk factor for endothelial dysfunction and that pravastatin improves endothelial function in individuals with isolated low HDL cholesterol through, at least in part, an increase in circulating progenitor cells.
Databáze: OpenAIRE