Peptidergic modulation of in situ canine intrinsic cardiac neurons

In order to determine which peptides are involved in modulating intrinsic cardiac neurons, angiotensin II, atrial natriuretic peptide, bradykinin, calcitonin gene-related peptide, enkephalin, neuropeptide Y, oxytocin, substance P, and vasoactive intestinal peptide dissolved in saline were administer...

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Published inPeptides (New York, N.Y. : 1980) Vol. 14; no. 2; pp. 191 - 202
Main Authors Armour, J.A., Huang, M.H., Smith, F.M.
Format Journal Article
LanguageEnglish
Published New York, NY Elsevier Inc 01.03.1993
Elsevier Science
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Summary:In order to determine which peptides are involved in modulating intrinsic cardiac neurons, angiotensin II, atrial natriuretic peptide, bradykinin, calcitonin gene-related peptide, enkephalin, neuropeptide Y, oxytocin, substance P, and vasoactive intestinal peptide dissolved in saline were administered individually by microinjection adjacent to spontaneously active canine intrinsic cardiac neurons. No neuronal or cardiac responses were elicited when saline was administered into active loci or when peptides were administered into loci with no spontaneous activity. Each peptide elecited neuronal responses when administered into active loci in most animals, bradykinin eliciting neuronal responses in every active locus studied. Concomitant cardiovascular responses were elicited in many cases when every peptide except atriopeptin was studied. After cardiac decentralization, neuronal and cardiovascular responses to repeat doses of peptides occurred with less frequency than before decentralization, implying that connections with central and other intrathoracic neurons can influence the function of peptide-sensitive intrinsic cardiac neurons. After atropine and timolol administration, cardiovascular, but not neuronal, responses to peptides were eliminated, indicating that cardiovascular responses were dependent upon efferent parasympathetic and sympathetic neurons. It is concluded that a number of neuropeptides may be involved in regulation of cardiac function by intrinsic cardiac neurons.
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ISSN:0196-9781
1873-5169
DOI:10.1016/0196-9781(93)90029-G