PMID- 12106662
OWN - NLM
STAT- MEDLINE
DCOM- 20021011
LR  - 20190614
IS  - 0006-8993 (Print)
IS  - 0006-8993 (Linking)
VI  - 944
IP  - 1-2
DP  - 2002 Jul 19
TI  - Substance P release in the feline nucleus tractus solitarius during ergoreceptor 
      but not baroreceptor afferent signaling.
PG  - 19-31
AB  - 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.
FAU - Williams, Carole A
AU  - Williams CA
AD  - Department of Physiology, College of Medicine, East Tennessee State University, 
      Johnson City, TN 37614-0576, USA. williams@etsu.edu
FAU - Reifsteck, Angela
AU  - Reifsteck A
FAU - Hampton, Toby A
AU  - Hampton TA
FAU - Fry, Bonnie
AU  - Fry B
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
PL  - Netherlands
TA  - Brain Res
JT  - Brain research
JID - 0045503
RN  - 0 (Neurokinin-1 Receptor Antagonists)
RN  - 0 (Receptors, Neurokinin-1)
RN  - 129623-01-4 (GR 82334)
RN  - 2507-24-6 (Physalaemin)
RN  - 33507-63-0 (Substance P)
SB  - IM
MH  - Afferent Pathways/drug effects/*metabolism
MH  - Animals
MH  - Baroreflex/drug effects/physiology
MH  - Cardiovascular Physiological Phenomena/drug effects
MH  - Cats
MH  - Mechanoreceptors/drug effects/*metabolism
MH  - Movement/drug effects/physiology
MH  - Muscle Contraction/drug effects/physiology
MH  - Muscle Fatigue/drug effects/physiology
MH  - Muscle, Skeletal/*innervation/physiology
MH  - Neural Inhibition/drug effects/physiology
MH  - Neurokinin-1 Receptor Antagonists
MH  - Neurons/cytology/drug effects/*metabolism
MH  - Physalaemin/*analogs & derivatives/pharmacology
MH  - Pressoreceptors/drug effects/*metabolism
MH  - Receptors, Neurokinin-1/metabolism
MH  - Solitary Nucleus/cytology/drug effects/*metabolism
MH  - Substance P/*metabolism
MH  - Sympathetic Nervous System/cytology/drug effects/metabolism
EDAT- 2002/07/11 10:00
MHDA- 2002/10/12 04:00
CRDT- 2002/07/11 10:00
PHST- 2002/07/11 10:00 [pubmed]
PHST- 2002/10/12 04:00 [medline]
PHST- 2002/07/11 10:00 [entrez]
AID - S0006899302026422 [pii]
AID - 10.1016/s0006-8993(02)02642-2 [doi]
PST - ppublish
SO  - Brain Res. 2002 Jul 19;944(1-2):19-31. doi: 10.1016/s0006-8993(02)02642-2.