IQUIMEFA   05518
INSTITUTO QUIMICA Y METABOLISMO DEL FARMACO
Unidad Ejecutora - UE
artículos
Título:
Enhanced Assymetrical Noradrenergic Transmission
Autor/es:
TAMARA ABRAMOFF; MARÍA J. GUIL; VANINA P. MORALES; SANDRA I. HOPE; CELESTE SORIA; LILIANA G. BIANCIOTTI; MARCELO S. VATTA
Revista:
NEUROCHEMICAL RESEARCH
Editorial:
SPRINGER/PLENUM PUBLISHERS
Referencias:
Lugar: New York; Año: 2013 vol. 38 p. 2063 - 2071
ISSN:
0364-3190
Resumen:
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