Nitric oxide (NO) is produced in the vascular system by endothelial nitric oxide synthase (eNOS), a Ca+2/calmodulin (CaM)-dependent enzyme. NO production is promoted by diverse agonists that transiently increase intracellular Ca+2 concentration and activate eNOS. For example, interaction of eNOS with caveolin, the structural scaffolding protein of caveolae reduces eNOS activity. The calveolin-eNOS complex undergoes cycles of association and dissociation modulated by Ca+2 concentrations. Other regulators of eNOS action include HSP90 and Akt which synergistically increase eNOS activity along with formation of a ternary complex comprised of HSP90, Akt, and CaM-bound eNOS...