Lin S S, Chan J Y, Chan S H
Institute of Pharmacology, National Yang-Ming Medical College, Taipei, Taiwan, Republic of China.
Regul Pept. 1991 May 17;33(3):239-50. doi: 10.1016/0167-0115(91)90227-8.
We evaluated the potential participation of endogenous brain somatostatin-14 (SOM) in central cardiovascular regulation, using adult male Sprague-Dawley rats anesthetized with pentobarbital sodium (40 mg/kg, i.p.). Intracerebroventricular (i.c.v.) application of SOM (2 or 4 nmol) promoted a significant elevation in baroreceptor reflex (BRR) response, induced by phenylephrine (5 micrograms kg, i.v.). Blocking the endogenous SOM activity with its specific receptor antagonist, cyclo-[7-aminoheptanoyl-Phe-D-Trp-Lys-Thr(Bzl)] (2 or 4 nmol, i.c.v.) or antiserum against SOM (1:20, i.c.v.), on the other hand, appreciably attenuated the same response. These modulatory effects on the BRR response were essentially duplicated upon bilateral microinjections of SOM (320 pmol), SOM antagonist (320 pmol) or anti-SOM (1:20) into the caudal portion of the nucleus of tractus solitarius (NTS), the terminal site for baroreceptor afferents. These results suggest that neurons that contain SOM may participate in cardiovascular control by tonically facilitating the BRR, possibly by exerting an influence on the neurons 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，评估内源性脑生长抑素-14（SOM）在中枢心血管调节中的潜在作用。脑室内（i.c.v.）注射SOM（2或4nmol）可使去氧肾上腺素（5μg/kg，静脉注射）诱导的压力感受器反射（BRR）反应显著增强。另一方面，用其特异性受体拮抗剂环-[7-氨基庚酰-Phe-D-Trp-Lys-Thr（Bzl）]（2或4nmol，i.c.v.）或抗SOM血清（1:20，i.c.v.）阻断内源性SOM活性，可明显减弱相同反应。在孤束核（NTS）尾端（压力感受器传入神经的终末部位）双侧微量注射SOM（320pmol）、SOM拮抗剂（320pmol）或抗SOM（1:20）后，对BRR反应的这些调节作用基本重现。这些结果表明，含有SOM的神经元可能通过持续促进BRR参与心血管控制，可能是通过对NTS的神经元施加影响来实现的。
