Chan J Y, Lin S S, Chan S H
Department of Medical Research, Veterans General Hospital-Taipei, Taiwan, Republic of China.
Neurosci Lett. 1992 Jan 6;134(2):267-70. doi: 10.1016/0304-3940(92)90532-c.
We evaluated the transmembrane signaling mechanism that may underlie the facilitatory action of somatostatin (SOM) on baroreceptor reflex (BRR), using adult, male, Sprague-Dawley rats anesthetized with pentobarbital sodium (40 mg/kg, i.p.). Intracerebroventricular (i.c.v.) application of SOM (2 nmol) promoted a significant elevation in BRR response, induced by phenylephrine (5 micrograms/kg, i.v.). This potentiatory action of the tetradecapeptide was significantly reversed after pretreating animals with bilateral microinjection of pertussis toxin (25 ng) or N-ethylmaleimide (2 nmol) into the nucleus tractus solitarius (NTS), the terminal site for baroreceptor afferents. These results suggest that a pertussis toxin-sensitive GTP-binding regulatory protein, possibly Gi, may be involved in the modulation of the BRR by SOM at the NTS.
我们使用戊巴比妥钠（40mg/kg，腹腔注射）麻醉的成年雄性Sprague-Dawley大鼠，评估了可能是生长抑素（SOM）对压力感受器反射（BRR）促进作用基础的跨膜信号传导机制。脑室内（i.c.v.）注射SOM（2nmol）可促进由去氧肾上腺素（5μg/kg，静脉注射）诱导的BRR反应显著升高。在用百日咳毒素（25ng）或N-乙基马来酰亚胺（2nmol）双侧微量注射到孤束核（NTS）（压力感受器传入神经的终末部位）预处理动物后，这种十四肽的增强作用被显著逆转。这些结果表明，一种对百日咳毒素敏感的GTP结合调节蛋白，可能是Gi，可能参与了SOM在NTS对BRR的调节。
