The role of nitric oxide derived from L-arginine in the control of steroidogenesis, and perfusion medium flow rate in the isolated perfused rat adrenal gland.

The present studies were designed to investigate the role of nitric oxide (NO) in the regulation of adrenocortical function, using the intact rat adrenal gland in situ, perfused with medium (Hank's balanced salt solution) containing a range of concentrations of L-arginine, the substrate for NO production. In addition, the effects of NG-nitro-L-arginine methylester (L-NAME), an inhibitor of NO production, were investigated. Results showed that L-arginine caused a dose-dependent increase in the flow rate of the perfusion medium through the adrenal gland. This effect was specific, as neither D-arginine nor L-lysine had an effect. The presence of L-NAME (5 mmol/l) in perfusion medium containing L-arginine caused a decrease in flow rate to levels in the absence of L-arginine. In the presence of concentrations of L-arginine up to 500 mumol/l, corticosterone secretion rates were also stimulated in a dose-dependent manner. Further studies, investigating the effect of L-arginine on the response to ACTH(1-24) stimulation, found that the percentage increase in flow rate, aldosterone secretion and corticosterone secretion caused by ACTH were not significantly different using media containing 230 mumol L-arginine/l or in the absence of L-arginine. These results suggest a role for NO derived from L-arginine in the regulation of basal levels of adrenal vascular tone in the rat isolated adrenal gland preparation. They do not suggest an obligatory role for NO in either the vascular or steroidogenic response to ACTH stimulation.