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Vol. 283, Issue 2, 478-487, 1997
Department of Pharmacology, Shinshu University School of Medicine,
Matsumoto 390, Japan
We investigated the effects of a neuropeptide, pituitary adenylate
cyclase-activating polypeptide- (PACAP) 27, on the sinoatrial nodal
pacemaker activity and the mechanisms for the cardiac effects of
PACAP-27 in the autonomically decentralized heart of the anesthetized dog. PACAP-27 (0.01-0.3 nmol) injected into the sinus node artery increased followed by decreased sinus rate. PACAP-27 (0.1 and 0.3 nmol)
caused atrial fibrillation spontaneously. After atropine, PACAP-27
never decreased but only increased sinus rate as did vasoactive
intestinal peptide. However, propranolol did not affect the negative
and positive chronotropic effects. Tetrodotoxin but not hexamethonium
abolished the negative chronotropic response to PACAP-27 in atropine
nontreated dogs, and tetrodotoxin also inhibited the positive
chronotropic response by 34% in atropine-treated dogs. In atropine-
and propranolol-treated dogs, positive chronotropic responses to
PACAP-27 were inhibited by PACAP-(6-27), a PACAP receptor antagonist
but not by vasoactive intestinal peptide (10-28), a vasoactive
intestinal peptide receptor antagonist. These results indicate that
PACAP-27 causes the negative chronotropic effect through the
postganglionic parasympathetic nerve activation and it produces the
positive chronotropic effect mediated by PACAP receptors with an
activation of non-adrenergic, nonvasoactive intestinal peptide-ergic
nerves at least in part in the dog heart. Atropine and tetrodotoxin
abolished atrial fibrillation induced by PACAP-27 but other blockers
did not. These results suggest that neurally released acetylcholine
induced by PACAP-27 participates in the induction of atrial
fibrillation.
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