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For the prevention of angina pectoris due to coronary artery disease and the treatment of acute and chronic angina pectoris, hypertension, and myocardial infarction.
Similar to other nitrites and organic nitrates, Isosorbide Mononitrate is converted to nitric oxide (NO), an active intermediate compound which activates the enzyme guanylate cyclase (Atrial natriuretic peptide receptor A). This stimulates the synthesis of cyclic guanosine 3',5'-monophosphate (cGMP) which then activates a series of protein kinase-dependent phosphorylations in the smooth muscle cells, eventually resulting in the dephosphorylation of the myosin light chain of the smooth muscle fiber. The subsequent release of calcium ions results in the relaxation of the smooth muscle cells and vasodilation.
Symptoms of overdose include vasodilatation, venous pooling, reduced cardiac output, and hypotension. There are no data suggesting what dose of isosorbide mononitrate is likely to be life-threatening in humans. In rats and mice, there is significant lethality at doses of 2000 mg/kg and 3000 mg/kg, respectively.
100%
5 hours
Isosorbide mononitrate is primarily metabolized by the liver, but unlike oral isosorbide dinitrate, it is not subject to first-pass metabolism. Isosorbide mononitrate is cleared by denitration to isosorbide and glucuronidation as the mononitrate, with 96% of the administered dose excreted in the urine within 5 days and only about 1% eliminated in the feces. At least six different compounds have been detected in urine, with about 2% of the dose excreted as the unchanged drug and at least five metabolites.
* 0.6 to 0.7 L/kg
* 120–122 mL/min [Single dose of 60 mg PO] * 151–187 mL/min [Single dose of extended-release tablet 60 mg PO] * 132-151 mL/min [Multiple doses of extended release tablet 60 mg PO] * 119-140 mL/min [Multiple doses of extended release tablet 120 mg PO]