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Cardiovascular effects of L-glutamate and gamma-aminobutyric acid injected into the rostral ventrolateral medulla in normotensive and spontaneously hypertensive rats.
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1986
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HypertensionChemical StimulationCardiovascular PharmacologyAnesthetic MechanismGlutamate-sensitive SitesExperimental PharmacologySocial SciencesHypertensive RatsNeurochemistryRostral Ventrolateral MedullaBilateral MicroinjectionsAnesthetic PharmacologyCardiovascular EffectsAntihypertensive TherapyVascular PharmacologyNeuropharmacologyNervous SystemPharmacologyAnaesthetic AgentNeurophysiologyPhysiologyElectrophysiologyAnesthesiaMedicineAnesthesiology
We studied the responses to chemical stimulation of the ventrolateral medulla in pentobarbital-anaesthetized, paralyzed, normotensive and spontaneously hypertensive (SHR) rats. When unilaterally injected into a circumscribed region of the rostral ventrolateral medulla, L-glutamate (0.16-1.6 nmol) elicited a dose-dependent increase in arterial pressure and heart rate. Bilateral microinjections of L-glutamate diethylester (63 nmol), an antagonist of excitatory amino acids, into the glutamate-sensitive sites markedly reduced arterial pressure and heart rate. gamma-Aminobutyric acid (GABA) (0.3-3 nmol) injected into the glutamate-sensitive sites caused a dose-dependent decrease in arterial pressure and heart rate. The depressor response to GABA was smaller in SHR than that in normotensive Wistar Kyoto rats (WKY), while there were no differences between WKY and SHR in the pressor response to L-glutamate. Thus, a depressor function involving the ventrolateral medulla appears to be diminished in SHR.