PHARMACOLOGICAL PROFILE OF A NEW CORONARY VASODILATOR DRUG, 2-NICOTINAMIDOETHYL NITRATE (SG-75)

1. In anaesthetized, open‐chest dogs, 2‐nicotinamidoethyl nitrate (SG‐75) administered intravenously (0.3–1 mg/kg) or intraduodenally (3 mg/kg) produced decreases in systemic blood pressure, coronary resistance, heart rate and an increase in coronary sinus outflow, but virtually no change in myocardial oxygen consumption and atrioventricular conduction. The effects of SG‐75 administered intraduodenally emerged within a few minutes after dosing and lasted over about 1 h. 2. In isolated, blood‐perfused sino‐atrial node preparations of the dog SG‐75 administered into the sinus node artery decreased slightly sinus rate at the dose which doubled blood flow through the artery. 3. In isolated, blood‐perfused atrioventricular node preparations of the dog SG‐75 administered into the atrioventricular node artery did not impair atrioventricular conduction even in doses which increased blood flow through the artery to more than twice the basal level. 4. In isolated, blood‐perfused papillary muscle preparations of the dog SG‐75 administered into the anterior septal artery scarcely affected force of contraction of the papillary muscle at the dose which doubled blood flow through the artery, although in further large doses it produced a transient decrease in the force of contraction. In extremely large doses it produced ventricular fibrillation. 5. In anaesthetized, open‐chest dogs in which cardiac input was kept constant SG‐75 (0.01–1 mg/kg) administered into the ascending aorta increased venous return without changing systemic output. 6. 2‐Nicotinamidoethyl alcohol, a denitrated compound of SG‐75, had no vasodilator action in doses comparable to those of the parent compound. 7. These results indicate SG‐75 to be a potential antianginal drug having no cardiodepressant actions but having properties uncharacteristic of the nitrates. Copyright © 1979, Wiley Blackwell. All rights reserved