Portal de Periódicos da CAPES

Relaxation of rabbit aorta by chlordimeform

1984; Wiley; Volume: 4; Issue: 1 Linguagem: Inglês

10.1002/jat.2550040107

1099-1263

Casey P. Robinson,

Receptor Mechanisms and Signaling

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 × 10 −7 M prostaglandin F 2α were not altered by the antimuscarinic agent atropine (10 −5 M ), the beta ‐adrenergic antagonist propranolol (10 −5 M ), the histamine H 2 antagonist cimetidine (2 × 10 −4 M ), the dopamine antagonist haloperidol (10 −5 M ) or the Na + ‐K + ‐ATPase inhibitor ouabain (5 × 10 −6 M ). CDF further relaxed deadventitiated strips contracted by 10 −6 M NE or 40 m M 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.