The effect of moxonidine on plasma lipid profile and on LDL subclass distribution
Autor: | Alexandros D. Tselepis, C. Tzallas, C Petris, S.-A. Karabina, Elisaf, Eleni Bairaktari, Kostas C. Siamopoulos |
---|---|
Rok vydání: | 1999 |
Předmět: |
Adult
Male medicine.medical_specialty Sympathetic nervous system Lipoproteins LDL/*blood/metabolism Lipids/*blood Imidazoline receptor Blood Pressure Stimulation Pharmacology Copper/pharmacology Hypertension/*blood/*drug therapy Blood Pressure/drug effects Pathogenesis Oxidation-Reduction/drug effects Internal medicine Internal Medicine medicine Humans Treatment Failure Antihypertensive Agents Moxonidine business.industry Imidazoles Middle Aged Lipids Lipoproteins LDL Endocrinology Blood pressure medicine.anatomical_structure Mechanism of action Hypertension Imidazoles/*therapeutic use Female lipids (amino acids peptides and proteins) medicine.symptom business Oxidation-Reduction Antihypertensive Agents/*therapeutic use Copper medicine.drug Lipoprotein |
Zdroj: | Journal of Human Hypertension. 13:781-785 |
ISSN: | 1476-5527 0950-9240 |
DOI: | 10.1038/sj.jhh.1000835 |
Popis: | Moxonidine is a new antihypertensive agent whose mechanism of action appears to involve specific stimulation of imidazoline receptors resulting in an inhibition of the activity of the central and peripheral sympathetic nervous system. The drug seems to behave neutrally with respect to plasma lipid parameters. However, there are no data on the effects of moxonidine on the low-density lipoprotein (LDL) subclass pattern or on the LDL oxidation susceptibility, both of which are known to play a prominent role in the pathogenesis of atherosclerosis. Thus, we undertook the present study to examine the influence of moxonidine on the LDL subspecies profile and their susceptibility to copper-induced oxidative modification in 20 hypertensive patients (11 men, 9 women) aged 38-61 years. Moxonidine administered at a dose of 0.4 mg daily for 8 weeks produced a significant decrease in both systolic and diastolic blood pressure (from 147 +/- 10 to 131 +/- 11 mm Hg, P < 0.001, and from 98 +/- 4.5 to 86 +/- 5 mm Hg, P < 0.001, respectively). No significant change in plasma lipid profile was observed after moxonidine administration. Additionally, no change in the susceptibility of LDL subclasses to copper-induced oxidative modification was noticed. Finally, drug therapy was not followed by any change in either LDL phenotype or in mass and composition of the three LDL subfractions. We conclude, that unlike other antihypertensive drugs, such as beta-blockers which may predispose to expression of a relatively atherogenic lipoprotein subclass pattern, moxonidine does not affect either plasma lipid parameters or lipoprotein composition. J Hum Hypertens |
Databáze: | OpenAIRE |
Externí odkaz: |