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Enhanced assymetrical noradrenergic transmission in the olfactory bulb of deoxycorticosterone acetate-salt hypertensive rats.

Authors
  • Abramoff, Tamara
  • Guil, María J
  • Morales, Vanina P
  • Hope, Sandra I
  • Soria, Celeste
  • Bianciotti, Liliana G
  • Vatta, Marcelo S
Type
Published Article
Journal
Neurochemical Research
Publisher
Springer-Verlag
Publication Date
Oct 01, 2013
Volume
38
Issue
10
Pages
2063–2071
Identifiers
DOI: 10.1007/s11064-013-1114-0
PMID: 23888389
Source
Medline
License
Unknown

Abstract

The ablation of olfactory bulb induces critical changes in dopamine, and monoamine oxidase activity in the brain stem. Growing evidence supports the participation of this telencephalic region in the regulation blood pressure and cardiovascular activity but little is known about its contribution to hypertension. We have previously reported that in the olfactory bulb of normotensive rats endothelins enhance noradrenergic activity by increasing tyrosine hydroxylase activity and norepinephrine release. In the present study we sought to establish the status of noradrenergic activity in the olfactory bulb of deoxycorticosterone acetate (DOCA)-salt hypertensive rats. Different steps in norepinephrine transmission including tyrosine hydroxylase activity, neuronal norepinephrine release and uptake were assessed in the left and right olfactory bulb of DOCA-salt hypertensive rats. Increased tyrosine hydroxylase activity, and decreased neuronal norepinephrine uptake were observed in the olfactory bulb of DOCA-salt hypertensive rats. Furthermore the expression of tyrosine hydroxylase and its phosphorylated forms were also augmented. Intriguingly, asymmetrical responses between the right and left olfactory bulb of normotensive and hypertensive rats were observed. Neuronal norepinephrine release was increased in the right but not in the left olfactory bulb of DOCA-salt hypertensive rats, whereas non asymmetrical differences were observed in normotensive animals. Present findings indicate that the olfactory bulb of hypertensive rats show an asymmetrical increase in norepinephrine activity. The observed changes in noradrenergic transmission may likely contribute to the onset and/or progression of hypertension in this animal model.

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