Premium
Action of atrial natriuretic peptide (ANP) on dog cerebral arteries: evidence that neurogenic relaxation is not mediated by release of ANP
Author(s) -
Okamura Tomio,
Inoue Seiji,
Toda Noboru
Publication year - 1989
Publication title -
british journal of pharmacology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.432
H-Index - 211
eISSN - 1476-5381
pISSN - 0007-1188
DOI - 10.1111/j.1476-5381.1989.tb12587.x
Subject(s) - atrial natriuretic peptide , medicine , endocrinology , cerebral arteries , ouabain , tachyphylaxis , stimulation , contraction (grammar) , chemistry , prostaglandin , sodium , organic chemistry
1 Atrial natriuretic peptide (ANP) (10 −9 to 10 −8 m ) produced a concentration‐related relaxation in helical strips of dog cerebral arteries partially contracted with prostaglandin F 2α . The relaxation was not affected by treatment with ouabain, quinidine, oxyhaemoglobin, methylene blue, or removal of endothelium. 2 Relaxations induced by nicotine or transmural electrical stimulation were not reduced in arteries in which tachyphylaxis to ANP had developed. 3 In arteries exposed to Ca 2+ ‐free media under severe hypoxia, contractions due to prostaglandin F 2α and Ca 2+ were attenuated by treatment with ANP, whereas the reoxygenation‐induced contraction was unaffected. 4 The results suggest that ANP does not mediate neurogenic relaxation of dog cerebral arteries. The ANP‐induced relaxation is not associated with activation of the sodium pump but is due to an inhibitory action on the release and influx of Ca 2+ , probably as a result of stimulation of guanylate cyclase.