Relaxation of rabbit aorta by chlordimeform.

Abstract

Chlordimeform N'-(4-choro-O-tolyl)-N,N-dimethyl-formamidine; CDF), an acaracide-insecticide, relaxed helically cut strips of rabbit thoracic aorta and deadventitiated aorta strips. Relaxations by CDF of aorta strips contracted by 5 x 10(-7) M prostaglandin F2 alpha were not altered by the antimuscarinic agent atropine (10(-5) M), the beta-adrenergic antagonist propranolol (10(-5) M), the histamine H2 antagonist cimetidine (2 x 10(-4) M), the dopamine antagonist haloperidol (10(-5) M) or the Na+-K+-ATPase inhibitor ouabain (5 x 10(-6) M). CDF further relaxed deadventitiated strips contracted by 10(-6) M NE or 40 mM potassium and then partially relaxed by 10(-5) M verapamil. CDF (10(-5) M) potentiated contractions caused by the addition of calcium to potassium depolarized strips in zero calcium media, but higher concentrations reduced calcium-induced contractions. The highest CDF concentration (10(-2) M) not only prevented tension increase on calcium addition, but also progressively decreased tension to below baseline levels. The addition of 10(-2) M CDF to aorta strips not contracted by a vasoactive agent decreased resting tension. This relaxation was usually maximal at 10(-3) M and less at 10(-2) M. Thus, CDF relaxes vascular smooth muscle, not by antagonism at the usual vascular relaxant receptors, but by interference with calcium utilization.