Nitric oxide production in the vascular endothelium is promoted by diverse agonists that
transiently increase intracellular Ca 2+ concentration and activate the endothelial nitric-
oxide synthase (eNOS), a Ca 2+/calmodulin-dependent enzyme. eNOS is acylated by the
fatty acids myristate and palmitate and is targeted thereby to plasmalemmal signal-
transducing domains termed caveolae. eNOS enzyme activity is markedly attenuated by its
interactions with caveolin, the structural scaffolding protein of caveolae. We have discovered …