Effects of the L/N-Type Ca2+ Channel Blocker Cilnidipine on the Cardiac Histological Remodelling and Inducibility of Atrial Fibrillation in High-Salt-Fed Rats
| Autor: | Akira Takahara, Megumi Aimoto, Kazumi Sugino, Eri Harada |
|---|---|
| Rok vydání: | 2021 |
| Předmět: |
0301 basic medicine
Pharmacology medicine.medical_specialty business.industry Cardiac fibrosis Pharmaceutical Science Atrial fibrillation General Medicine Cilnidipine medicine.disease Muscle hypertrophy 03 medical and health sciences 030104 developmental biology 0302 clinical medicine Blood pressure Endocrinology Fibrosis 030220 oncology & carcinogenesis Internal medicine medicine Channel blocker Amlodipine business medicine.drug |
| Zdroj: | Biological and Pharmaceutical Bulletin. 44:707-713 |
| ISSN: | 1347-5215 0918-6158 |
| Popis: | High salt intake has been shown to induce hypertrophy and fibrosis in the atria and ventricles, which could result in the development of atrial fibrillation (AF). Whereas the development of AF is suggested to be prevented by renin-angiotensin system (RAS) inhibitors, recent findings have indicated that this prevention is closely associated with their antihypertensive effects. In this study, we investigated whether the L/N-type Ca2+ channel blocker cilnidipine counteracts salt-induced atrial and ventricular remodelling and the inducibility of AF. Cilnidipine was orally administered to Dahl salt-sensitive rats fed with an 8% NaCl diet at 10 mg/kg for 5 weeks, and then electrophysiological evaluation and histological analyses were performed. The effects were compared with those of the L-type Ca2+ channel blocker amlodipine at 3 mg/kg. Following the intake of the 8% NaCl diet, the blood pressure (BP) increased, and fibrosis was induced in the atria and ventricles. Cilnidipine decreased BP, and the extent of the decrease in the cilnidipine group was similar to those in the amlodipine group. Cilnidipine produced a greater decrease in the fibrotic area in the atria and ventricles than amlodipine. The cilnidipine group shortened the AF duration from 7.43 ± 3.16 to 2.95 ± 1.73 s, which had been increased by NaCl intake. Plasma noradrenaline levels in the cilnidipine group were lower than those in the amlodipine group. Thus, the suppressive effects of cilnidipine on the salt-induced atrial and ventricular remodelling, fibrosis, and AF sustainability might be closely associated with its N-type Ca2+ channel-blocking actions. |
| Databáze: | OpenAIRE |
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