Medullary pathways for adrenocorticotropic hormone and vasopressin secretion in rabbits.
We determined, in urethan-anesthetized rabbits, whether pharmacological alteration of neuronal function in the ventrolateral medulla oblongata, including the A1 area, and in the nucleus tractus solitarii (NTS), alters plasma adrenocorticotropic hormone (ACTH) and vasopressin and whether inhibition of neuronal function in the ventrolateral medulla impairs the secretion of ACTH normally observed in response to hemorrhage or constriction of the inferior vena cava. We also tested whether the increase in plasma ACTH and vasopressin after pharmacological inhibition of neuronal function in the NTS is dependent on a pathway that synapses in the A1 area of the ventrolateral medulla. Activation of the A1 area with bicuculline increased both ACTH and vasopressin. Inhibition of the NTS with muscimol increased levels of both hormones, as did hemorrhage and constriction of the inferior vena cava. Inhibition of neuronal function within the A1 area with muscimol eliminated the secretion of vasopressin but did not significantly alter the secretion of ACTH, obtained by injecting muscimol into the NTS. Injection of muscimol into the A1 area eliminated the secretion of both ACTH and vasopressin in response to constriction of the inferior vena cava and, in the case of vasopressin, in response to hemorrhage. Although hemorrhage-initiated secretion of ACTH was significantly reduced by injection of muscimol into the A1 area, it was not completely eliminated by these injections or by injections of muscimol into a more rostrocaudally extensive region of the medulla oblongata. We conclude that the net output from the NTS tonically inhibits secretion of both ACTH and vasopressin, reflecting tonic baroreceptor tone. For vasopressin, the pathway from the NTS to the hypothalamus is dependent on a synapse in the A1 area. For ACTH, there are pathways to the hypothalamus that do not synapse in the A1 area, but neurons in this region do have an excitatory effect on secretion of ACTH.
Gieroba
Z J
ZJ
Department of Medicine, Flinders University of South Australia, Bedford Park.
Fullerton
M J
MJ
Funder
J W
JW
Blessing
W W
WW
D015763:2-Amino-5-phosphonovalerate / Q000494:pharmacology; D000324:Adrenocorticotropic Hormone / Q000097:blood / Q000378:metabolism*; D000818:Animals; D002319:Cardiovascular System / Q000378:metabolism / Q000503:physiopathology; D003251:Constriction, Pathologic; D006470:Hemorrhage / Q000097:blood / Q000503:physiopathology; D006935:Hypercapnia / Q000378:metabolism / Q000503:physiopathology; D000860:Hypoxia / Q000378:metabolism / Q000503:physiopathology; D007267:Injections; D008526:Medulla Oblongata / Q000502:physiology*; D009118:Muscimol / Q000494:pharmacology; D011817:Rabbits; D013268:Stimulation, Chemical; D014667:Vasopressins / Q000097:blood / Q000378:metabolism*; D014682:Vena Cava, Inferior
D014667:Vasopressins; D009118:Muscimol; D015763:2-Amino-5-phosphonovalerate; D000324:Adrenocorticotropic Hormone