The mechanism of action of nitroglycerine in the management of angina pectoris is:
High-Yield Explanation
Ans: b (Post capillary venodilation)Ref Thripathi 5 ed., Pg. 489Nitroglycerine and other nitrates act by dilating veins more than arteries. This results in peripheral pooling of blood which leads decreased venous return. So the preload is reduced and eventually, decreased cardiac work.In variant angina - nitrates work by dilating the large coronary vessels.Mechanism of action of other antianginal drugsBeta blockers - they decrease heart rate, inotropic state and mean BP. This results in reduced cardiac work.Calcium channel blockers - it causes smooth muscle (vascular) relaxation and negative chronotropic, inotropic and dromotropic actionK+ channel openers - e.g., nicorandil. It causes smooth muscle relaxation.Dipyridamole - prevents uptake and degradation of adenosine. Adenosine is a vasodilator.Trimetazidine - it improves myocardial glucose utilization through inhibition of fatty acid metabolism (LC3- KAT inhibitor)Ranolazine - it inhibits late I current (funny current inhibitor). It also inhibits LC3- KAT.Notes on NitratesMOA - it is more venodilator than arteriolar dilator.Short acting - GlyceryltrinitrateNitroglycerineLong acting - Isosorbide dinitrate (short acting if sublingual)Isosorbide mononitrateAdverse effects- Headache Flushing, weakness, palpitation Methhemoglobinaemia RashesTolerance to the drug occurs if the drug is continuously present in the body.All except Isosorbide mononitrate undergo extensive firstpass metabolism in liver.