Clinical Study with Azelnidipine in Patients with Essential Hypertension
| Autor: | Jyunichi Mikawa, Tomohito Kawano, Teru Nada, Masahiro Nomura, Susumu Ito, Kunihiko Koshiba |
|---|---|
| Rok vydání: | 2011 |
| Předmět: |
medicine.medical_specialty
business.industry medicine.drug_class Azelnidipine Vasodilation Brain natriuretic peptide Essential hypertension medicine.disease Endocrinology Atrial natriuretic peptide Internal medicine Drug Discovery cardiovascular system medicine Natriuretic peptide Amlodipine business Pulse wave velocity medicine.drug |
| Zdroj: | Arzneimittelforschung. 57:698-704 |
| ISSN: | 1616-7066 0004-4172 |
| DOI: | 10.1055/s-0031-1296670 |
| Popis: | A dihydropyridine calcium (Ca) antagonist, azelnidipine (CAS 123524-52-7, Cal-block®), exhibits hypotensive effects for a prolonged duration, and has been reported to have a strong antiarteriosclerotic action due to its high affinity for vascular tissues and antioxidative action. It has also been reported that azelnidipine does not cause tachycardia associated with the baroreceptor reflex due to vasodilatation. In this study, the antiarteriosclerotic and cardiac hypertrophy-inhibitory effects, and the autonomic nervous activity in essential hypertension of azelnidipine were investigated. The study was performed using the following 2 protocols: 1) Pulse wave velocity (PWV), carotid arterial inti-ma media thickness (IMT), echocardiog-raphy, high sensitive C-reactive protein (hs-CRP), interleukin-6 (IL-6), tumor necrosis factor alpha (TNF-α), adiponectin, brain natriuretic peptide (BNP), and 8-isoprostane were measured after an initial treatment with azelnidipine. 2) The treatment was switched to azelnidipine in patients who had previously been under treatment with amlodipine for essential hypertension, and 123I-metaiodoben-zylguanidine myocardial scintigraphy (123I-MIBG), measurements of plasma norepinephrine, atrial natriuretic peptide (ANP), and BNP, Holter electrocardiogra-phy, and heart rate variability analysis were performed. PWV, IMT, hs-CRP, IL-6, and TNF-α significantly decreased. The levels of 8-isopros-tane, an antioxidative marker, were also significantly decreased, while adioponec-tin levels were significantly increased after the initial treatment with azelnid-ipine. After switching from amlodipine, azelnidipine exhibited a hypotensive effects comparable to amlodipine, and significantly decreased heart rate and the total number of extrasystoles. Noradrena-line levels and the LF/HF ratio were significantly decreased, and the washout rate was significantly reduced on 123I-MIBG myocardial scintigraphy. These findings suggest that azelnidipine inhibits the enhancement of sympathetic nervous activity and the progression of arteriosclerosis through its antioxidative effects. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|