Abstract
In the anesthetized rhesus monkey, thalicarpine (10 mg/kg), a dimeric alkaloid consisting of benzisoquinoline (veraisoquin, 10 mg/kg) and aporphine (N-methyl-laurotetanine, 10 mg/kg) moieties, depressed mean arterial pressure and force of contraction, but increased carotid artery blood flow and heart rate. N-methyl-laurotetanine depressed all four parameters, whereas veraisoquin increased the first three parameters. All three compounds produced an immediate negative inotropic and chronotropic response in isolated, blood-perfused dog hearts. After veraisoquin, heart rate and force of contraction increased above control levels within 5 min. Thalicarpine was the only agent which caused a persistent decrease in coronary perfusion pressure in this preparation. Many of the cardiovascular actions of thalicarpine can be ascribed to the aporphine moiety, but some appear to require the intact dimeric molecule.
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