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Dehydroepiandrosterone (DHEA) is an adrenal steroid hormone, which has the highest serum concentration among steroid hormones with DHEA sulfate (DHEAS). DHEA possesses an inhibitory action on glucose-6-phosphate dehydrogenase (G6PD), the first pentose-phosphate pathway enzyme that reduces NADP +  to NADPH. DHEA induced relaxation of high K + -induced contraction in rat arterial strips, whereas DHEAS barely induced it. We studied the effects of DHEA on L-type Ca 2+  current ( I Ca,L ) of A7r5 arterial smooth muscle cells and compared the mechanism of inhibition with that produced by the 6-aminonicotinamide (6-AN) competitive inhibitor of G6PD. DHEA moderately inhibited I Ca,L  that was elicited from a holding potential (HP) of −80 mV [voltage-independent inhibition (VIDI)] and accelerated decay of I Ca,L  during the depolarization pulse [voltage-dependent inhibition (VDI)]. DHEA-induced VDI decreased peak I Ca,L  at depolarized HPs. By applying repetitive depolarization pulses from multiple HPs, novel HP-dependent steady-state inactivation curves ( f ∞ -HP) were constructed. DHEA shifted f ∞ -HP to the left and inhibited the window current, which was recorded at depolarized HPs and obtained as a product of current-voltage relationship and f ∞ -HP. The IC 50  value of I Ca,L  inhibition was much higher than serum concentration. DHEA-induced VDI was downregulated by the dialysis of guanosine 5′- O-(2-thiodiphosphate), which shifted f ∞ -voltage to the right before the application of DHEA. 6-AN gradually and irreversibly inhibited I Ca,L  by VIDI, suggesting that the inhibition of G6PD is involved in DHEA-induced VIDI. In 6-AN-pretreated cells, DHEA induced additional inhibition by increasing VIDI and generating VDI. The inhibition of G6PD underlies DHEA-induced VIDI, and DHEA additionally induces VDI as described for Ca 2+  channel blockers.    NEW &amp; NOTEWORTHY Dehydroepiandrosterone, the most abundantly released adrenal steroid hormone with dehydroepiandrosterone sulfate, inhibited L-type Ca 2+  current and its window current in aortic smooth muscle cells. The IC 50  value of inhibition decreased with the depolarization of holding potential to 15 µM at −20 mV. The inhibition occurred in a voltage-dependent manner as described for Ca 2+  channel blockers and in a voltage-independent manner because of the inhibition of glucose-6-phosphate dehydrogenase.

american journal of physiology. heart and circulatory physiology

Dehydroepiandrosterone inhibits<i>I</i><sub>Ca,L</sub>and its window current in voltage-dependent and -independent mechanisms in arterial smooth muscle cells

Dehydroepiandrosterone inhibitsICa,Land its window current in voltage-dependent and -independent mechanisms in arterial smooth muscle cells

Dehydroepiandrosterone inhibitsI_Ca,Land its window current in voltage-dependent and -independent mechanisms in arterial smooth muscle cells