Akademik Veri Yönetim Sistemi
Bratislava Medical Journal, cilt.116, sa.5, ss.326-329, 2015 (SCI-Expanded)
Background: Elevated L-type Ca2+ channel expression level increases Ca2+ influx. This can cause hypertrophy and pathological remodeling of the heart especially under stress conditions. Nesfatin-1 can activate hypothalamic L, P and Q type Ca2+ channels and increase insulin secretion in pancreatic islet beta cells via activation of L-type Ca2+ channels. On the other hand, the effect of nesfatin-1 on cardiac L-type Ca2+ channels has not been studied yet. Objectives: We aimed to identify the effect of peripheral chronic nesfatin-1 application on cardiac L-type Ca2+ channel α1c subunit expression level in normal rats and those subjected to chronic restraint stress. Methods: Three-month aged Wistar albino rats were randomly divided into 4 groups (n = 7) as Control, Stress, Control+Nesfatin-1, and Nesfatin-1+Stress. Rats in groups subjected to restraint stress were placed in a specially built size-manipulable cabin for 2 h/day (between 10:00 and 12:00 a.m.) for 10 consecutive days without allowing water and food intake. Nesfatin-1 segment (0.25 nmol/g bw intraperitoneally) was applied during the 10 consecutive days. Western blot analyses were performed to determine the expression level of L-type Ca2+ channel α1c subunit protein in rat cardiac extracts. Results: Cardiac L-type Ca2+ channel α1c subunit protein expression levels were increased significantly after chronic peripheral nesfatin-1 application in rats subjected to restraint stress (p = 0.032). Conclusion: We can conclude that nesfatin-1 can cause cardiac failures during clinical treatments by elevating cardiac L-type Ca2+ channel α1c subunit protein expression level (Fig. 2, Ref. 26). Text in PDF www.elis.sk.