Pharmacology: Pharmacodynamics: Glyceryl trinitrate reduces the tone of vascular smooth muscle. This action is more marked on the venous capacitance vessels than the arterial vessels. There is a reduction in venous return to the heart and a lowering of elevated filling pressure. This lowering of filling pressure reduces the left ventricular end diastolic volume and preload. The net effect is a lowering of myocardial oxygen consumption. Systemic vascular resistance, pulmonary vascular pressure, and arterial pressure are also reduced by glyceryl trinitrate and there is a net reduction in the afterload. By reducing the preload and afterload, glyceryl trinitrate reduces the workload on the heart. Glyceryl trinitrate affects oxygen supply by redistributing blood flow along collateral channels from the epicardial to endocardial regions.
Pharmacokinetics: Biotransformation: As with all commonly used organic nitrates the metabolic degradation of glyceryl trinitrate occurs via denitration and glucuronidation. The less active metabolites resulting from this biotransformation can be recovered from the urine within 24 hours.
Elimination: Glyceryl trinitrate is eliminated from plasma with a short half-life of about 2-3 minutes. This rapid disappearance from plasma is consistent with the high systemic clearance values for this drug (up to 3,270 l/hour).