Oxytocin (OXT) is a peptide involved in diverse physiological functions in the central nervous system including central cardiovascular regulation. Previously it has been demonstrated that OXT microinjected in the nucleus tractus solitarii (NTS) elicits a dose-dependent increase of mean arterial pressure (MAP) and heart rate (HR). Moreover, OXT blocks the vasodepressor responses induced by α2-adrenergic agonists and decreases α2-adrenergic receptor binding within the NTS. The aim of this work was to investigate if the cardiovascular actions of OXT were mediated through specific OXT receptors and if OXT could modulate the cardiovascular responses elicited by L-glutamate, the main transmitter of the primary baroreceptor afferents.
Experiments were performed in urethane-anaesthetised rats, and animals received unilateral injection in the NTS in a total volume of 50 nl. Mean arterial pressure (MAP) and HR were recorded from the femoral artery over 30 min. To determine if the action of OXT is mediated by specific receptors, animals received microinjections of OXT (10 pmol) alone or together with the OXT-selective antagonist receptor d(CH2)5,Tyr(Me)2,Orn8-vasotocin (OXA) (10 pmol). These results were analysed using one-way ANOVA followed by Fisher’s post test. To test the possible modulation of OXT on the cardiovascular response induced by L-glutamate (L-Glu) other groups of rats received coinjections of a threshold dose of OXT (1 pmol) plus an ED50 dose of L-Glu (1.5 nmol), or with threshold doses of both OXT (1 pmol) and L-Glu (30 pmol). These results were analysed using Student’s unpaired t test. Control rats received CSF alone. At the end of the experiments, the rats were humanely killed.
The presence of OXA blocked the vasopressor response of OXT. This blockade was partial (P < 0.05) in the first 15 min of recording but complete (P < 0.001) when it was analysed for the 30 min recording period. However, OXA significantly blocked the tachycardic response of OXT (P < 0.01) immediately after coinjections. With regard to the modulation of L-Glu responses, threshold doses of OXT significantly blocked (P < 0.001) the vasodepressor responses elicited by the ED50 dose of L-Glu by 80 %, without any modification of its bradycardic effect. Coinjections of threshold doses of OXT and L-Glu did not produce any change in MAP values, but elicited a bradycardia.
These results demonstrate that cardiovascular actions of OXT in the NTS are mediated by specific OXT receptors and suggest an involvement of OXT on the modulation of baroreceptor reflex within the NTS.
This work has been supported by the Spanish CICYT (BFI2001-1905).