title: The release of inhibitory amino acids in the hypothalamus is tonically modified by impulses from aortic baroreceptors as a consequence of blood pressure fluctuations.
abstract: We investigated in conscious, freely moving rats whether the release of GABA, taurine and arginine in the hypothalamus is influenced by impulses originating from peripheral baroreceptors. The posterior hypothalamic nucleus was superfused with artificial cerebrospinal fluid through a push-push cannula and the release of amino acids was determined in the hypothalamic superfusate of control rats, as well as of rats after bilateral aortic denervation (AD). AD led to hypertension and increased the lability of arterial pressure. In sham-operated rats, intravenous infusion of phenylephrine increased blood pressure and the hypothalamic release of GABA and taurine. AD almost abolished the phenylephrine-induced release of the inhibitory amino acids. Similarly, the pressor response to hypervolaemia, elicited by blood injection, enhanced the release rates of GABA and taurine only in sham-operated rats. Baroreceptor unloading evoked either by intravenous infusion of nitroprusside, or by haemorrhage, decreased the release rates of GABA and taurine in sham-operated rats but not in AD rats. Electrical stimulation of the afferent aortic depressor nerve enhanced extracellular GABA and taurine in the posterior hypothalamic nucleus. The release rate of arginine was not influenced by alterations in baroreceptor activity either in sham-operated or in AD rats. The findings support the idea that, in the hypothalamus, GABA and taurine are involved in central blood pressure regulation. The release of these two amino acids seems to be driven tonically by baroreceptor impulses. Moreover, the findings indicate that the baroreceptors of the aortic arch play a crucial role in the mediation of changes in hypothalamic GABA and taurine outflow so as to counteract blood pressure fluctuations.
authors.affiliation: Institut für Pharmakologie und Toxikologie der Universität Innsbruck, Austria.
authors.forename: N
authors.initials: N
authors.lastname: Singewald
authors.forename: D
authors.initials: D
authors.lastname: Kouvelas
authors.forename: F
authors.initials: F
authors.lastname: Chen
authors.forename: A
authors.initials: A
authors.lastname: Philippu
mesh_terms: D000596:Amino Acids / Q000378:metabolism*; D000818:Animals; D001011:Aorta / Q000294:innervation*; D001120:Arginine / Q000378:metabolism; D001794:Blood Pressure / Q000502:physiology*; D001810:Blood Volume / Q000502:physiology*; D003714:Denervation; D004558:Electric Stimulation; D007031:Hypothalamus / Q000378:metabolism*; D008297:Male; D009599:Nitroprusside / Q000494:pharmacology; D010656:Phenylephrine / Q000494:pharmacology; D011311:Pressoreceptors / Q000502:physiology*; D051381:Rats; D017207:Rats, Sprague-Dawley; D013654:Taurine / Q000378:metabolism; D014662:Vasoconstrictor Agents / Q000494:pharmacology; D005680:gamma-Aminobutyric Acid / Q000378:metabolism
chemical_list: D000596:Amino Acids; D014662:Vasoconstrictor Agents; D009599:Nitroprusside; D013654:Taurine; D010656:Phenylephrine; D005680:gamma-Aminobutyric Acid; D001120:Arginine