Grundemar L, Wahlestedt C, Reis D J
Department of Neurology, Cornell University Medical College, New York, NY 10021.
Neurosci Lett. 1991 Jan 14;122(1):135-9. doi: 10.1016/0304-3940(91)90211-b.
Neuropeptide Y (NPY) microinjected unilaterally into the nucleus tractus solitarii (NTS) of anesthetized paralyzed rats elicits a gradual dose-dependent and reversible fall in arterial pressure (AP) and heart rate (HR) lasting 20 min. It also abolished the brief (less than 1 min) dose-dependent and reversible fall of AP and HR elicited by L-glutamate (L-Glu) injected into the nucleus. The blockade of L-Glu by NPY appeared gradually and was prolonged, lasting over 2 h, and recovering by 24 h. It was not replicated by desamido-NPY or galanin. Unlike 2% lidocaine it did not block the hypotension elicited by focal electrical stimulation at the injection site indicating the response was not that of a local anesthetic. Bilateral injection of NPY into the NTS resulted, after an initial fall, in an elevation of AP (+48 +/- 10.6 mmHg). At this time the reflex bradycardia evoked by elevating AP with phenylephrine was markedly reduced. We conclude that in the NTS, NPY antagonizes the actions of L-Glu and may attenuate baroreceptor reflexes. Since the NTS is richly innervated by NPY neurons and contains many NPY binding sites and since primary baroreceptor afferents appear to be glutamatergic the results suggested that NPY may serve in NTS as a long-term regulator of baroreceptor reflex activity.
向麻醉的瘫痪大鼠孤束核（NTS）单侧微量注射神经肽Y（NPY）会引起动脉血压（AP）和心率（HR）逐渐呈剂量依赖性且可逆的下降，持续20分钟。它还消除了向该核团注射L-谷氨酸（L-Glu）所引起的AP和HR短暂（少于1分钟）的剂量依赖性且可逆的下降。NPY对L-Glu的阻断作用逐渐出现且持续时间延长，超过2小时，并在24小时恢复。脱酰胺NPY或甘丙肽无法复制这种作用。与2%利多卡因不同，它不会阻断注射部位局部电刺激所引起的低血压，表明该反应并非局部麻醉药的作用。向NTS双侧注射NPY，在最初的血压下降后，会导致AP升高（+48±10.6 mmHg）。此时，用去氧肾上腺素升高AP所诱发的反射性心动过缓明显减弱。我们得出结论，在NTS中，NPY拮抗L-Glu的作用，并可能减弱压力感受器反射。由于NTS由NPY神经元大量支配且含有许多NPY结合位点，并且由于初级压力感受器传入神经似乎是谷氨酸能的，因此结果表明NPY在NTS中可能作为压力感受器反射活动的长期调节因子。
