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J.Health Sci., 46(6), 455-458, 2000
Lipids, Lipoproteins and Fibrinolytic Parameters During Amlodipine Treatment of Hypertension
Joseph Eberendu Ahaneku,*, a, 1 Kazuyuki Sakata,c Tetsumei Urano,a Yumiko Takada,b and Akikazu Takada a
aDepartment of Physiology and bDepartment of Pathophysiology, Hamamatsu University School of Medicine, 3600, Handa-cho, Hamamatsu-shi, Shizuoka 431-3192, Japan, and cDepartment of Cardiology, Shizuoka General Hospital, 4-27-1, Kita-andou, Shizuoka-shi, Shizuoka 420-0881, Japan
In order to determine the safety or otherwise of amlodipine, we evaluated lipid and lipoprotein indices as well as fibrinolytic parameters in Japanese hypertensive patients undergoing amlodipine treatment. Lipids, lipoproteins, tissue plasminogen activator (t-PA), total and free plasminogen activator inhibitor-1 (PAI-1) and t-PA-PAI-1 complexes were determined in twenty-seven patients with essential hypertension before and after 3 months of amlodipine treatment. Plasma renin and noradrenaline levels were also determined. The mean systolic and diastolic blood pressures and heart rate were reduced, while the plasma renin and noradrenaline levels remained unchanged after amlodipine therapy. Triglycerides, very low density lipoprotein- cholesterol (VLDLC), total and free PAI-1 levels were significantly reduced, while the levels of total cholesterol (TC), high density lipoprotein-cholesterol (HDLC), low density lipoprotein-cholesterol (LDLC), HDLC/TC ratio, t-PA and t-PA-PAI-1 complex did not change from their pretreatment values after amlodipine treatment. There was a significant positive correlation between HDLC and t-PA-PAI-1 complex levels after amlodipine treatment. The findings from the present study show that amlodipine is effective for the treatment of hypertension and does not cause reflex tachycardia in Japanese patients. We also found that amlodipine treatment is a safe antihypertensive agent characterized by beneficial lipid changes and enhanced fibrinolysis in Japanese hypertensive patients. The direct relationship between lipid levels and fibrinolytic function seen in this study has added to our understanding and knowledge of the pathogenesis of atherosclerosis during antihypertensive pharmacotherapy.
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