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      Cardiovascular effects of L-glutamate microinjection in the supraoptic nucleus of unanaesthetized rats.

      Neuropharmacology
      Animals, Arginine Vasopressin, analogs & derivatives, blood, pharmacology, Blood Pressure, drug effects, Excitatory Amino Acid Antagonists, Ganglionic Blockers, Glutamic Acid, administration & dosage, Heart Rate, Isoquinolines, Male, Microinjections, Pentolinium Tartrate, Quinoxalines, Rats, Rats, Wistar, Supraoptic Nucleus, physiology, Vasopressins, metabolism

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          Abstract

          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.

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