Glucocorticoid modulation of atrial natriuretic peptide, oxytocin, vasopressin and Fos expression in response to osmotic, angiotensinergic and cholinergic stimulation.
The regulation of fluid and electrolyte homeostasis involves the participation of several neuropeptides and hormones that utilize hypothalamic cholinergic, alpha-adrenergic and angiotensinergic neurotransmitters and pathways. Additionally, it has been suggested that hypothalamus-pituitary-adrenal axis activity modulates hormonal responses to blood volume expansion. In the present study, we evaluated the effect of dexamethasone on atrial natriuretic peptide (ANP), oxytocin (OT) and vasopressin (AVP) responses to i.c.v. microinjections of 0.15 M and 0.30 M NaCl, angiotensin-II (ANG-II) and carbachol. We also evaluated the Fos protein immunoreactivity in the median preoptic (MnPO), paraventricular (PVN) and supraoptic (SON) nuclei. Male Wistar rats received an i.p. injection of dexamethasone (1 mg/kg) or vehicle (0.15 M NaCl) 2 h before the i.c.v. microinjections. Blood samples for plasma ANP, OT, AVP and corticosterone determinations were collected at 5 and 20 min after stimulus. Another set of rats was perfused 120 min after stimulation. A significant increase in plasma ANP, OT, AVP and corticosterone levels was observed at 5 and 20 min after each central stimulation compared with isotonic saline-injected group. Pre-treatment with dexamethasone decreased plasma corticosterone and OT levels, with no changes in the AVP secretion. On the other hand, dexamethasone induced a significant increase in plasma ANP levels. A significant increase in the number of Fos immunoreactive neurons was observed in the MnPO, PVN and SON after i.c.v. stimulations. Pre-treatment with dexamethasone induced a significant decrease in Fos immunoreactivity in these nuclei compared with the vehicle. These results indicate that central osmotic, cholinergic, and angiotensinergic stimuli activate MnPO, PVN and SON, with a subsequent OT, AVP, and ANP release. The present data also suggest that these responses are modulated by glucocorticoids.
Lauand
F
F
Department of Physiology, School of Medicine of Ribeirao Preto, University of Sao Paulo, Avenida dos Bandeirantes, 3900 Monte Alegre, CEP 14049-900 Ribeirao Preto, SP, Brazil.
Ruginsk
S G
SG
Rodrigues
H L P
HL
Reis
W L
WL
de Castro
M
M
Elias
L L K
LL
Antunes-Rodrigues
J
J
D000222:Adaptation, Physiological; D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D009320:Atrial Natriuretic Factor / Q000097:blood* / Q000187:drug effects; D002217:Carbachol / Q000494:pharmacology; D018679:Cholinergic Agonists / Q000494:pharmacology; D003345:Corticosterone / Q000097:blood; D003907:Dexamethasone / Q000494:pharmacology; D005938:Glucocorticoids / Q000494:pharmacology; D007031:Hypothalamus / Q000166:cytology / Q000187:drug effects / Q000502:physiology*; D007276:Injections, Intraventricular; D008297:Male; D010121:Oxytocin / Q000097:blood* / Q000187:drug effects; D016760:Proto-Oncogene Proteins c-fos / Q000187:drug effects / Q000378:metabolism; D051381:Rats; D017208:Rats, Wistar; D013268:Stimulation, Chemical; D014667:Vasopressins / Q000097:blood* / Q000187:drug effects; D014882:Water-Electrolyte Balance / Q000502:physiology*
D018679:Cholinergic Agonists; D005938:Glucocorticoids; D016760:Proto-Oncogene Proteins c-fos; D014667:Vasopressins; D000804:Angiotensin II; D010121:Oxytocin; D003907:Dexamethasone; D009320:Atrial Natriuretic Factor; D002217:Carbachol; D003345:Corticosterone