Electrophysiologic studies have demonstrated that adrenal medulla chromaffin cells express voltage-dependent P/Q-, N-, L-, and R-type Call channels and that these channels regulate release of norepinephrine and epinephrine. However, N-type Ca2+ channel alpha(1B)-deficient mice with a CBA/JN background show normal plasma norepinephrine and epinephrine levels, presumably owing to compensation by other gene(s). To examine the expression patterns of the P/Q-type alpha(1A) L-type alpha(1C)/alpha(1D) and R-type alpha(1E), beta(1), beta(2), beta(3) and beta(4) subunits, as well as of tyrosine hydroxylase (Th), dopamine beta hydroxylase (Dbh), and phenylethanolamine-N-methyltransferase (Pnmt) in the adrenal gland of alpha(1B)-deficient mice, we used real-time quantitative reverse transcription-polymerase chain reaction and Western blot analyses. The expression levels of alpha(1A), beta(4), Th, and Th phosphorylated at serine 40 were higher in homozygous mice than in wild-type and heterozygous mice, but the expression levels of alpha(1C), alpha(1D), alpha(1E), beta(1), beta(2), beta(3), Dbh, and Pnmt did not differ among wild-type, heterozygous, and homozygous mice. These results suggest that the compensatory mechanisms to maintain normal levels of epinephrine and norepinephrine in the adrenal gland of N-type Ca2+ channel alpha(1B)-deficient mice include increased expression of alpha(1A) and beta(4) subunits and increased catecholamine biosynthetic activity.