III. Hormonal regulation of phosphatidylinositol breakdown

Cyclic AMP and Ca²⁺ are intracellular mediators of hormone action. Catecholamines interact with beta adrenoceptors to activate adenylate cyclase or with alpha₂ adrenoceptors to inhibit adenylate cyclase. Alpha₁ adrenoceptor activation results in elevation of cytosol Ca²⁺ and an increased breakdown of phosphatidylinositol. In blowfly salivary glands, 5-hydroxytryptamine (5-HT) interacts with beta type receptors resulting in adenylate cyclase activation while alpha type receptors are involved in phosphatidylinositol breakdown and elevation of cytosol Ca²⁺. The link between Ca²⁺ mobilization and phosphatidylinositol breakdown remains to be established but breakdown of the receptor-regulated pool of phosphatidylinositol is not secondary to the rise in Ca²⁺. Direct addition of 5-HT to cell-free homogenates of blowfly salivary glands results in activation of phosphatidylinositol breakdown in the absence of Ca²⁺. In rat liver plasma membrane preparations, vasopressin increases phosphatidylinositol breakdown in the absence of Ca²⁺ or cytosol if deoxycholate is present. The data do not indicate whether hormone activation increases the availability of substrate to enzymatic hydrolysis or activates phospholipase C. However, they demonstrate that hormones directly accelerate phosphatidylinositol breakdown.