Jawaharlal Nehru Technological University Hyderabad B.Pharmacy III Year PHARMACOLOGY-II Previous Question Paper (August/September-2021 - R17)

The electrophysiology of the heart is governed by the generation and conduction of action potentials. Cardiac cells are classified into fast-response fibers (atrial and ventricular myocytes, Purkinje fibers) and slow-response fibers (SA and AV nodes). The action potential of a ventricular myocyte consists of five phases: Phase 0 (Rapid depolarization) due to Na+ influx; Phase 1 (Initial rapid repolarization) due to K+ efflux; Phase 2 (Plateau phase) due to Ca2+ influx balancing K+ efflux; Phase 3 (Final rapid repolarization) due to K+ efflux; and Phase 4 (Resting membrane potential) maintained by the Na+/K+ ATPase pump. The SA node exhibits pacemaker activity characterized by a slow spontaneous diastolic depolarization (Phase 4) driven by the funny current (If) and T-type Ca2+ channels.

Anti-anginal drugs are classified into: 1. Organic Nitrates (Nitroglycerin, Isosorbide dinitrate), 2. Beta-blockers (Propranolol, Atenolol), 3. Calcium Channel Blockers (Verapamil, Amlodipine), and 4. Potassium channel openers (Nicorandil). The mechanism of action involves reducing myocardial oxygen demand or increasing oxygen supply. Nitrates act by releasing nitric oxide (NO) in vascular smooth muscle, increasing cGMP, leading to venodilation and reduced preload. Beta-blockers reduce heart rate and contractility by blocking beta-1 receptors, thereby decreasing myocardial oxygen consumption. Calcium channel blockers inhibit L-type calcium channels, causing coronary vasodilation and reducing cardiac contractility. Nicorandil acts as a dual agent by opening ATP-sensitive potassium channels and providing a nitrate-like effect, resulting in both arterial and venous dilation.