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1 Faculdade de Odontologia de Ribeirão Preto, 2 Escola de Enfermagem de Ribeirão Preto, and 3 Faculdade de Medicina de Ribeirão Preto, Universidade de São Paulo, 14040-904 Ribeirão Preto, São Paulo, Brazil
It has been reported that arginine
vasopressin (AVP) plays a thermoregulatory action, but very little is
known about the mechanisms involved. In the present study, we tested
the hypothesis that nitric oxide (NO) plays a role in systemic
AVP-induced hypothermia. Rectal temperature was measured before and
after AVP, AVP blocker, or
NG-nitro-L-arginine methyl ester
(L-NAME; NO synthase inhibitor) injection. Control animals received saline injections of the same volume. The basal body temperature
(Tb) measured in control animals was 36.53 ± 0.08°C. We observed a significant
(P < 0.05) reduction in
Tb to 35.44 ± 0.19°C after
intravenous injection of AVP (2 µg/kg) and to 35.74 ± 0.10°C
after intravenous injection of
L-NAME (30 mg/kg). The systemic
injection of the AVP blocker
[
-mercapto-
,
-cyclopentamethylenepropionyl1,O-Et-Tyr2,Val4,Arg8]vasopressin
(10 µg/kg) caused a significant increase in
Tb to 37.33 ± 0.23°C,
indicating that AVP plays a tonic role by reducing Tb. When the treatments with AVP
and L-NAME were combined,
systemically injected L-NAME
blunted AVP-induced hypothermia. To assess the role of central
thermoregulatory mechanisms, a smaller dose of L-NAME (1 mg/kg) was injected
into the third cerebral ventricle. Intracerebroventricular injection of
L-NAME caused an increase in
Tb, but when
intracerebroventricular L-NAME
was combined with systemic AVP injection (2 µg/kg), no change in
Tb was observed. The data indicate
that central NO plays a major role mediating systemic AVP-induced
hypothermia.
endothelium-derived relaxing factor; temperature; nitric oxide synthase; arginine vasopressin
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