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Energy conservation by nisoldipine in ischaemic heart
Author(s) -
Jong Jan W.,
Huizer Tom,
Tijssen Jan G.P.
Publication year - 1984
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1984.tb16535.x
Subject(s) - nisoldipine , chemistry , perfusion , adenylate kinase , vasodilation , pharmacology , medicine , high energy phosphate , energy charge , calcium , endocrinology , biochemistry , energy metabolism , phosphocreatine , receptor , nifedipine
1 We studied the effect of the calcium entry blocker nisoldipine on ATP catabolism in the rat heart, perfused according to Langendorff. Even 1 n M nisoldipine induced vasodilatation; concentrations of 30 n M and higher caused significant negative inotropy. 2 The drug had a very strong affinity for silicon rubber tubing. 3 Myocardial ischaemia was induced by lowering the perfusion pressure, which reduced flow without nisoldipine by 85%. The efflux of purine nucleosides and oxypurines rose 14 fold. Nisoldipine reduced this efflux of ATP catabolites dose‐dependently. The highest concentration, 300 n M , suppressed ischaemic purine production completely. 4 The action of the drug was antagonized by an increase in Ca 2+ ‐concentration in the perfusion fluid. 5 We also showed the protective effect of nisoldipine on adenine nucleotides in freeze‐clamped hearts. A concentration of 20 n M partially prevented the reduction of ATP and adenylate energy charge due to ischaemia. 6 We conclude that relatively low doses of nisoldipine effectively prevent ATP breakdown in ischaemic rat heart.