Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Pivot Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Target Concepts:
Gene/Protein
Disease
Symptom
Drug
Enzyme
Compound
Query: EC:3.4.24.59 (
MIP
)
4,906
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
In animals and man the antidysrhythmic agent disopyramide in primarily metabolised by mono-N-dealkylation. The effects of disopyramide and its N-dealkylated metabolite (
MIP
) have been investigated using isolated cardiac and nervous tissue, and their effects have been compared with the effects of other antidysrhythmic agents. Disopyramide, d,l-propranolol and quinidine all decreased both maximum driving frequency and developed tension in electrically driven guinea pit atria.
MIP
and procaine amide also decreased maximum driving frequency, but had a positive intropic effect.
MIP
was only 4 times less active than disopyramide in decreasing maximum driving frequency. There was no evidence that either disopyramide or
MIP
possessed beta-adrenoceptor antagonist properties. In superfused rat sciatic nerves, it has been shown that neither disopyramide nor
MIP
possesses significant local anaesthetic properties.
Procaine amide
and lignocaine were highly active in this test. The possible contribution of
MIP
to the actions of disopyramide in vivo is discussed.
...
PMID:Some effects of disopyramide and its N-dealkylated metabolite on isolated nerve and cardiac muscle. 66 10
