Abstract
Biotin and its analog, (+)-biotin-p-nitrophenyl ester enhanced guanylate cyclase activity two- to threefold in rat liver, kidney, colon, cerebellum, and heart. Dose-response relationships revealed that at concentrations as low as 1 micromolar, both biotin and its analog caused maximal augmentation of guanylate cyclase activity. These data suggest a role for the activation of guanylate cyclase in the mechanism of action of this vitamin.