Ward D G, Baertschi A J, Gann D S
Am J Physiol. 1977 Sep;233(3):R116-26. doi: 10.1152/ajpregu.1977.233.3.R116.
To examine hindbrain pathways mediating release of adrenocorticotropin (ACTH) in response to hemodynamic changes we tested, in 19 cats (chloralose/urethan), 70 neurons in ACTH-active areas of the medulla for their response to volume pulsation (+/- 1 ml, 1 Hz, 60 s) of the right atrium (RA) or to hemorrhage (3 ml/kg per 30 s), and to electrical stimulation in ACTH-active areas of the dorsal rostral pons (DRP). The activity of 16 neurons was increased (P less than 0.05) by RA. Of these, 6 were driven antidromically from the locus subcoeruleus (LSC), and were located in the lateral solitary nucleus and in posteromedial nucleus intercalatus (NI). The activity of 11 neurons was decreased by RA. Of these, 5 were driven antidromically from LSC and lateral ventral tegmental nucleus and were located in anterolateral NI. No rostral projections were found to more medial sites in DRP. Responses to the first trial of RA were rapid, but slowed and attenuated with repeated trials. Responses to hemorrhage were rapid and in the opposite direction, but did not attenuate. The results suggest that pathways displaying rate sensitivity project from the right atrium via B-receptors to the DRP.