Singewald N, Kouvelas D, Chen F, Philippu A
Institut für Pharmakologie und Toxikologie der Universität Innsbruck, Austria.
Naunyn Schmiedebergs Arch Pharmacol. 1997 Sep;356(3):348-55. doi: 10.1007/pl00005061.
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.
我们在清醒、自由活动的大鼠中研究了下丘脑γ-氨基丁酸(GABA)、牛磺酸和精氨酸的释放是否受外周压力感受器传来的冲动影响。通过推挽式套管将人工脑脊液灌流到下丘脑后核,测定对照大鼠以及双侧主动脉去神经支配(AD)大鼠下丘脑灌流液中氨基酸的释放。AD导致高血压并增加动脉血压的不稳定性。在假手术大鼠中,静脉输注去氧肾上腺素可升高血压,并增加下丘脑GABA和牛磺酸的释放。AD几乎消除了去氧肾上腺素诱导的抑制性氨基酸释放。同样,注射血液引起的对高血容量的升压反应仅在假手术大鼠中提高了GABA和牛磺酸的释放率。静脉输注硝普钠或出血引起的压力感受器卸载降低了假手术大鼠而非AD大鼠中GABA和牛磺酸的释放率。电刺激主动脉减压神经传入纤维可增强下丘脑后核细胞外GABA和牛磺酸的含量。在假手术大鼠或AD大鼠中,精氨酸的释放率均不受压力感受器活动改变的影响。这些发现支持以下观点:在下丘脑中,GABA和牛磺酸参与中枢血压调节。这两种氨基酸的释放似乎受压力感受器冲动的持续驱动。此外,这些发现表明主动脉弓压力感受器在介导下丘脑GABA和牛磺酸外流变化以抵消血压波动方面起关键作用。