This study shows that NO inhibits basal, ACTH and Angll-induced aldosterone synthesis in bovine adrenal glomerulosa cells. This inhibition is independent of soluble guanylyl cyclases cGMP levels, protein kinase G activity, cAMP production or phospholipase C activity. NO inhibits aldosterogenesis through, at least, a direct inhibition of cytochrome P450 steroidogenic enzymes, including P450scc enzyme activity. We present evidence that NO can be synthesized endogenously, since we have partially characterized NO synthase activity in glomeralosa cells extracts. In conclusion, our results support the hypothesis that NO can act as autocrine and/or paracrine modulator of aldosterone secretion from adrenal gland, thus contributing to the regulation of physiological aldosterone levels induced by hormones such as angiotensin II or ACTH.