Action of atrial natriuretic peptide (ANP) on dog cerebral arteries: evidence that neurogenic relaxation is not mediated by release of ANP.
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 F2 alpha. 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 Ca2+-free media under severe hypoxia, contractions due to prostaglandin F2 alpha and Ca2+ 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 Ca2+, probably as a result of stimulation of guanylate cyclase.
Okamura
T
T
Department of Pharmacology, Shiga University of Medical Sciences, Ohtsu, Japan.
Inoue
S
S
Toda
N
N
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology* / Q000502:physiology; D002118:Calcium / Q000494:pharmacology; D002536:Cerebral Arteries / Q000187:drug effects; D015237:Dinoprost / Q000494:pharmacology; D004285:Dogs; D004558:Electric Stimulation; D005260:Female; D066298:In Vitro Techniques; D007537:Isometric Contraction / Q000187:drug effects; D008297:Male; D009126:Muscle Relaxation / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects*; D014664:Vasodilation / Q000187:drug effects
D009320:Atrial Natriuretic Factor; D015237:Dinoprost; D002118:Calcium