Patent ductus arteriosus remodels cardiac sensory neuronal chemotransduction.
We sought to determine the capacity of neonatal ventricular sensory nerve endings (neurites) to transduce the cardiac milieu in the presence of cardiovascular pathology. The spontaneous activity generated by nodose ganglion cardiac afferent neurons was identified in situ using extracellular recording techniques in two groups of piglets approximately 2 weeks old: (i). controls that underwent sham operations (n=19 piglets) 2 weeks earlier and (ii). a pathological model of patent ductus arteriosus stented open for about 2 weeks (n=16 piglets). The capacity of ventricular sensory neurites associated with nodose ganglion afferent neurons to transduce local mechanical (including alterations in right or left ventricular volumes) or chemical stimuli was studied in both groups. The average conduction velocity of afferent axons associated with identified neuronal somata was estimated to be 1.5+/-0.6 or 2.9+/-1.3 m s(-1). Ventricular afferent neurons transduced mechanical stimuli similarly in both groups. In control animals, ventricular afferent neurons transduced the following chemicals: the sodium channel modifier veratridine (delta 23+/-7 impulses min(-1)), the P(1)-purinoceptor agonist adenosine (Delta 24+/-8 impulses min(-1)), and the beta-adrenoceptor agonist isoproterenol (delta 18+/-7 impulses min(-1)). On the other hand, patent ductus arteriosus cardiac afferent neurons did not transduce these chemicals. It is concluded that neonatal cardiac afferent neuronal chemosensory-as opposed to mechanosensory-transduction remodels in the presence of a patent ductus arteriosus. The reduced capacity of neonatal cardiac afferent neurons to transduce chemicals in the presence of a patent ductus arteriosus should be taken into account when considering neonatal cardiovascular control in such a state.
Chen
Robert P-C
RP
Department of Pediatrics, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia, Canada B3H 4H7. robert.chen@iwk.nshealth.ca
Thompson
Gregory W
GW
Armour
J Andrew
JA
D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000241:Adenosine / Q000494:pharmacology; D000318:Adrenergic beta-Agonists / Q000494:pharmacology; D000375:Aging / Q000502:physiology; D000818:Animals; D000831:Animals, Newborn; D002628:Chemoreceptor Cells / Q000187:drug effects / Q000254:growth & development*; D004195:Disease Models, Animal; D004374:Ductus Arteriosus, Patent / Q000503:physiopathology*; D005260:Female; D006352:Heart Ventricles / Q000254:growth & development / Q000294:innervation*; D008297:Male; D008465:Mechanoreceptors / Q000187:drug effects / Q000254:growth & development; D009431:Neural Conduction / Q000187:drug effects / Q000502:physiology; D009620:Nodose Ganglion / Q000187:drug effects / Q000254:growth & development*; D010812:Physical Stimulation; D011984:Sensory Receptor Cells / Q000187:drug effects / Q000254:growth & development; D015398:Signal Transduction / Q000187:drug effects / Q000502:physiology*; D026941:Sodium Channel Blockers / Q000494:pharmacology; D034421:Sus scrofa; D017833:Visceral Afferents / Q000187:drug effects / Q000254:growth & development*
D000318:Adrenergic beta-Agonists; D026941:Sodium Channel Blockers; D000241:Adenosine