Article

Azelnidipine inhibits aldosterone synthesis and secretion in human adrenocortical cell line NCI-H295R.

Department of Internal Medicine, Division of Diabetes and Endocrinology, Jikei University School of Medicine,Tokyo, Japan.
European journal of pharmacology (impact factor: 2.59). 02/2009; 605(1-3):49-52. DOI:10.1016/j.ejphar.2008.12.041 pp.49-52
Source: PubMed

ABSTRACT Blockade of a mineralocorticoid receptor is a clinically useful approach to the prevention of cardiovascular disease. The present study was designed to evaluate the effect of azelnidipine, a unique dihydropyridine Ca(2+) channel blocker, on aldosterone production in the human adrenocortical cell line NCI-H295R. Azelnidipine inhibited angiotensin II- and KCl-induced expression of steroid 11beta-hydroxylase, steroid 18-hydroxylase, and the alpha1H subunit of the T-type Ca(2+) channel, and suppressed steroid biosynthesis in H295R cells by the same amount as efonidipine. On the basis of these findings, azelnidipine appears to suppress steroid biosynthesis in H295R cells beyond the blockade of L-type calcium channels.

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Keywords

aldosterone production
 
alpha1H subunit
 
Azelnidipine inhibited angiotensin II-
 
cardiovascular disease
 
clinically useful approach
 
efonidipine
 
human adrenocortical cell line NCI-H295R
 
L-type calcium channels
 
steroid 11beta-hydroxylase
 
steroid 18-hydroxylase
 
steroid biosynthesis
 
suppressed steroid biosynthesis
 
unique dihydropyridine Ca(2+)