Propranolol is a a beta blocker. In the heart it acts as a receptor antagonist of beta-1-adrenergic receptor. Propranolol competes with neurotransmitters for receptors, which inhibits sympathetic stimulation of the heart. The reduction of neurotransmitters binding to beta receptor proteins in the heart inhibits adenylate cyclase type 1. Because adenylate cyclase type 1 typically activates cAMP synthesis, which in turn activates PKA production, which then activates SRC and nitric oxide synthase, its inhibition causes the inhibition cAMP, PKA, SRC and nitric oxide synthase. Following this chain of reactions, we see that the inhibition of nitric oxide synthase reduces nitric oxide production outside the cell which results in vasoconstriction. On a different end of this reaction chain, the inhibition of SRC in essence causes the activation of Caspase 3 and Caspase 9. This Caspase cascade leads to cell apoptosis. The net result of all these reactions is a decreased sympathetic effect on cardiac cells, causing the heart rate to slow and arterial blood pressure to lower. As a result, propranolol is used to treat hypertension, angina, migraine headaches, and hypertrophic subaortic stenosis.

Propranolol References