{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
{{facet.count}}
Restrict the search for
isosorbide mononitrate
to a specific field?
Glyceryl 2-nitrate (G-2-N) is the major metabolite of glyceryl trinitrate. Strips of rat aorta contracted with potassium chloride or with norepinephrine were relaxed by G-2-N. After oral administration to the anaesthetized rat or to the conscious dog G-2-N exhibited antianginal and hypotensive activity. The hypotensive and also cardiovascular activity of G-2-N lasted much longer than that of glyceryl trinitrate.
Glyceryl 1-nitrate (G-1-N) is an intermediate metabolic product in the stepwise de-esterification of glyceryl trinitrate (GTN) in animals and humans. It belongs to the group of orally effective longacting antianginal nitrates. In anesthetized rabbits, intravenous (L) G-1-N reduced the blood pressure slightly more than (D) G-1-N, while in the conscious dog the blood pressure lowering effect of (D) G-1-N was greater and had a much longer duration (4-6 versus 2 h) than that of (L)G-1-N. The differences in dogs are probably explained by enantiospecific pharmacokinetics: (D) G-1-N had higher plasma levels and showed a longer half-life of elimination than (L) G-1-N. From the pharmacokinetic point of view, the drug offers clear advantage over glyceryl trinitrate in clinical use: G-1-N is orally available - owing to its relatively low clearance it stays much longer in the body than GTN - kinetic parameters are predictable with low coefficients of variation - and the denitration products of G-1-N are expected to be pharmacologically neutral.