Enhancement of metabolic coronary vasodilatation by nicotinic acid or amide.
Cardiostimulation produced by noradrenaline, glucagon, or tachycardia on the isolated perfused rat heart produced a metabolic coronary dilatation that was potentiated by nicotinic acid or its amide [NIC; 0.05-1.0 mM] without affecting the cardiostimulation. Reactive hyperaemia to brief coronary occlusion was unaffected by NIC, thus confirming that its vasodilator mechanism is of a different nature than that leading to metabolic coronary dilatation. It is suggested that NIC may be of significance as an adjuvant in the treatment of certain types of coronary insufficiencies.
D000818:Animals; D003326:Coronary Circulation / Q000187:drug effects*; D003331:Coronary Vessels / Q000187:drug effects; D005934:Glucagon / Q000494:pharmacology; D006339:Heart Rate / Q000187:drug effects; D066298:In Vitro Techniques; D008297:Male; D009525:Niacin / Q000494:pharmacology*; D009536:Niacinamide / Q000494:pharmacology*; D009638:Norepinephrine / Q000494:pharmacology; D051381:Rats; D011919:Rats, Inbred Strains; D014664:Vasodilation / Q000187:drug effects*
D009536:Niacinamide; D009525:Niacin; D005934:Glucagon; D009638:Norepinephrine