Further evidence for the involvement of cyclic AMP in Ca2+-dependent, but not Ca2+-independent, noradrenaline release in the rabbit pulmonary artery.
Strips of the rabbit pulmonary artery were incubated with 3H-noradrenaline and subsequently superfused. In strips superfused with Ca2+-free solution containing K+ 64.7 mmol/l, tritium overflow was stimulated by introduction of Ca2+ 1.6 mmol/l; in strips superfused with physiological salt solution, stimulation was carried out with veratridine 30 mumol/l, acetylcholine 1 mmol/l (in the presence of atropine 1 mumol/l) or tyramine 100 mumol/l. The Ca2+-, veratridine- or acetylcholine-induced tritium overflow was facilitated by forskolin, AH 21-132 (a cAMP phosphodiesterase inhibitor) and/or 8-Br-cAMP, i.e. compounds which increase intraneuronal cAMP content. In contrast, the Ca2+-independent tyramine-evoked tritium overflow was not affected by these drugs. It is concluded that cAMP is involved in the regulation of stimulation-evoked Ca2+-dependent noradrenaline release, and that the sympathetic nerve terminals are endowed with an adenylate cyclase system. Facilitation of release may be caused by an alteration of Ca2+ influx or utilization.
D000109:Acetylcholine / Q000494:pharmacology; D000818:Animals; D002118:Calcium / Q000502:physiology*; D005576:Colforsin / Q000494:pharmacology; D000242:Cyclic AMP / Q000502:physiology*; D005260:Female; D066298:In Vitro Techniques; D008297:Male; D009119:Muscle Contraction / Q000187:drug effects; D009131:Muscle, Smooth, Vascular / Q000187:drug effects / Q000378:metabolism*; D009287:Naphthyridines / Q000494:pharmacology; D009638:Norepinephrine / Q000378:metabolism*; D010477:Perfusion; D010726:Phosphodiesterase Inhibitors / Q000494:pharmacology; D011651:Pulmonary Artery; D011817:Rabbits; D014701:Veratridine / Q000494:pharmacology
D009287:Naphthyridines; D010726:Phosphodiesterase Inhibitors; D005576:Colforsin; D014701:Veratridine; C044843:AH 21-132; D000242:Cyclic AMP; D000109:Acetylcholine; D002118:Calcium; D009638:Norepinephrine