Article ID | Journal | Published Year | Pages | File Type |
---|---|---|---|---|
2494883 | Neuropharmacology | 2007 | 7 Pages |
We report on the cardiovascular effects of l-glutamate (l-glu) microinjection in the hypothalamic supraoptic nucleus (SON) as well as possible receptor and mechanisms involved. Microinjection of l-glu in 100 nL in the SON caused dose-related pressor and bradycardic responses in unanesthetized rats. Responses were markedly reduced in urethane-anesthetized rats. The response to l-glu 10 nmol was blocked by local pretreatment with 2 nmol of the non-NMDA-receptors antagonist NBQX and not affected by 2 nmol of the selective NMDA-receptor antagonist LY 235959, suggesting that non-NMDA receptors mediate these responses. The pressor and bradycardic response to l-glu was potentiated by intravenous pretreatment with the ganglion blocker pentolinium and was blocked by intravenous pretreatment with the V1-vasopressin receptor antagonist dTyr(CH2)5(Me)AVP, suggesting involvement of circulating vasopressin in this response. Additionally l-glu microinjection into the SON increased plasma vasopressin levels (control: 1.3 ± 0.2 pg/mL, n = 6; l-glu: 14.7 ± 2.3 pg/mL, n = 6). In conclusion the results suggest that pressor responses to SON microinjection of l-glu are caused by activation of non-NMDA glutamate receptors and mediated by vasopressin release into systemic circulation.