title: Is the aortic depressor nerve involved in arterial chemoreflexes in rats?
abstract: Recent anatomical and physiological studies showed that chemoreceptor afferent fibers are present in the rat aortic depressor nerve (ADN), which has been considered to contain exclusively baroreceptor afferent fibers. However, it remains to be proven whether the chemoreceptor afferents of the ADN are practically involved in chemoreflexes. The present study was performed in chloralose/urethane-anesthetized rats of either Sprague-Dawley (SD) or Wistar strain to examine whether the ADN carries sufficient information regarding arterial hypoxia and hypercapnia, and whether the ADN indeed participates in chemoreflexes, the circulatory and respiratory components. It was found in either strain that afferent discharges of the ADN were not affected at all by hypoxia or hypercapnia, whereas those of the carotid sinus nerve (CSN) markedly increased due to these stimuli. Hypoxia produced hypertension, transient bradycardia followed by tachycardia, and respiratory facilitation, which characterize the chemoreflexes. Any of these responses was not affected at all by the ADN section, but all were abolished by the CSN section. Intraaortic injection of cyanide also induced transient bradycardia and respiratory facilitation, but any of them was not affected by the ADN section while all were abolished by the CSN section. Furthermore, electrical stimulation of the ADN produced solely baroreflex responses, i.e. hypotension and respiratory suppression, whereas that of the CSN provoked chemoreflex responses, i.e. early, transient hypertension and respiratory facilitation. In conclusion, the rat ADN does not contain a functionally significant number of chemoreceptor afferent fibers, if at all, and does not appreciably contribute to generation of chemoreflexes.
authors.affiliation: Department of Physiology, Mie University School of Medicine, Tsu, Japan. m-koba@doc.medic.mie-u.ac.jp
authors.forename: M
authors.initials: M
authors.lastname: Kobayashi
authors.forename: Z B
authors.initials: ZB
authors.lastname: Cheng
authors.forename: K
authors.initials: K
authors.lastname: Tanaka
authors.forename: S
authors.initials: S
authors.lastname: Nosaka
mesh_terms: D000200:Action Potentials / Q000187:drug effects / Q000502:physiology; D000818:Animals; D001011:Aorta / Q000294:innervation*; D001784:Blood Gas Analysis; D001794:Blood Pressure; D002344:Carotid Body / Q000187:drug effects / Q000502:physiology*; D002346:Carotid Sinus / Q000294:innervation*; D004558:Electric Stimulation; D006339:Heart Rate; D006935:Hypercapnia / Q000503:physiopathology; D000860:Hypoxia / Q000503:physiopathology; D008297:Male; D011042:Poisons / Q000494:pharmacology; D011311:Pressoreceptors / Q000187:drug effects / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D017208:Rats, Wistar; D012018:Reflex / Q000502:physiology; D012119:Respiration; D012966:Sodium Cyanide / Q000494:pharmacology
chemical_list: D011042:Poisons; D012966:Sodium Cyanide