title: Substance P release in the feline nucleus tractus solitarius during ergoreceptor but not baroreceptor afferent signaling.
abstract: Substance P (SP) is associated with metabo- and mechanoreceptor afferent fibers ('ergoreceptors') in skeletal muscle as well as the afferent fibers from carotid sinus baroreceptors. Afferent activity from each of these are at least partially integrated in the nucleus tractus solitarius (NTS). The purpose of this study was to determine whether SP was released from the NTS during acute reflex-induced changes in blood pressure caused by stimulating these receptors. Both the muscle pressor response and the baroreflex were studied in adult cats anaesthetized with alpha-chloralose. SP antibody-coated microprobes were used to measure the possible release of SP from the NTS. The muscle pressor response caused a release of immunoreactive SP-like substances (irSP) from the rostral medial NTS, as well as the dorsal motor nucleus (DMV) and lateral tegmental field (FTL). This release was not dependent on intact afferent input from the carotid sinus nerve, but was a function of activation of muscle ergoreceptors, since no irSP was released in response to stimulation of the motor nerves after the muscle was paralyzed. There was no detectable release of irSP from the mNTS during carotid artery occlusions (baroreceptor unloading). Baroreceptor activation, induced by the i.v. injection of the vasoconstrictor, phenylephrine, did not cause the release of irSP from the mNTS above resting baseline levels. These data suggest that SP is involved with the mediation of the afferent signal from muscle ergoreceptor fibers in the medial NTS. SP is not involved with the mediation of baroreceptor afferent signaling in the medial NTS. The release of SP in response to ergoreceptors activation may function to excite an inhibitory pathway which inhibits baroreflex signals that would tend to reduce the blood pressure and heart rate during the muscle pressor response.
authors.affiliation: Department of Physiology, College of Medicine, East Tennessee State University, Johnson City, TN 37614-0576, USA. williams@etsu.edu
authors.forename: Carole A
authors.initials: CA
authors.lastname: Williams
authors.forename: Angela
authors.initials: A
authors.lastname: Reifsteck
authors.forename: Toby A
authors.initials: TA
authors.lastname: Hampton
authors.forename: Bonnie
authors.initials: B
authors.lastname: Fry
mesh_terms: D000344:Afferent Pathways / Q000187:drug effects / Q000378:metabolism*; D000818:Animals; D017704:Baroreflex / Q000187:drug effects / Q000502:physiology; D002320:Cardiovascular Physiological Phenomena / Q000187:drug effects; D002415:Cats; D008465:Mechanoreceptors / Q000187:drug effects / Q000378:metabolism*; D009068:Movement / Q000187:drug effects / Q000502:physiology; D009119:Muscle Contraction / Q000187:drug effects / Q000502:physiology; D018763:Muscle Fatigue / Q000187:drug effects / Q000502:physiology; D018482:Muscle, Skeletal / Q000294:innervation* / Q000502:physiology; D009433:Neural Inhibition / Q000187:drug effects / Q000502:physiology; D064729:Neurokinin-1 Receptor Antagonists; D009474:Neurons / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D010803:Physalaemin / Q000031:analogs & derivatives* / Q000494:pharmacology; D011311:Pressoreceptors / Q000187:drug effects / Q000378:metabolism*; D018040:Receptors, Neurokinin-1 / Q000378:metabolism; D017552:Solitary Nucleus / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D013373:Substance P / Q000378:metabolism*; D013564:Sympathetic Nervous System / Q000166:cytology / Q000187:drug effects / Q000378:metabolism
chemical_list: D064729:Neurokinin-1 Receptor Antagonists; D018040:Receptors, Neurokinin-1; C079014:GR 82334; D010803:Physalaemin; D013373:Substance P