Neuropharmacological study on central peptidergic regulation of sympatho-adrenomedullary system.

从我们最近对蛙皮素引起的胃酸分泌中枢抑制机制的研究中，有人认为交感神经系统或肾上腺髓质系统的功能障碍可以很好地由功能未改变的系统补偿。然后，脑室内应用蛙皮素（i. c. v.）使用尿烷酯化大鼠，从神经药理学角度检测了对血浆儿茶酚胺水平的影响。所得结果如下。1)蛙皮素i. c. v.剂量依赖性地（0.3-10 nmole）增加肾上腺素（AD）和去甲肾上腺素（NA）的血浆水平[对照：AD; 170 ± 28，NA; 429 ± 33 pg/ml（n=20）。3 nmole蛙皮素30分钟后：AD; 1145 ± 247，NA 719 ± 162 pg/ml（n=50）]。使用6-羟基多巴胺的化学交感神经切除术显著增强了蛙皮素诱导的AD水平的增加[3 nmol蛙皮素后30分钟; 3600 ± 357 pg/ml（n=5）]。手术肾上腺切除术不影响蛙皮素诱导的NA水平的增加。2)电刺激蛙皮素作用的中心部位视前区，可增加AD和NA的水平，与蛙皮素相同。3)蛙皮素诱导的AD水平增加而非NA水平增加的出现时间通过用α-肾上腺素受体阻断剂酚妥拉明（s.c.）但β-肾上腺素受体阻滞剂心得安就不行4)静脉输注尼古丁可使内脏大切除大鼠的AD和NA水平升高。结果提示，交感神经系统在AD分泌的调节机制中具有抑制作用。此外，这种调节机制的位点可能存在于大脑中，而不是在外周靶器官肾上腺中。

From our recent studies on a mechanism of bombesin-induced central inhibition of gastric acid secretion, it was suggested that a dysfunction of the sympathetic or of the adrenomedullary system may well be compensated for by the system with unaltered function. Then, effects of bombesin intracerebroventricularaly applied (i.c.v.) on the plasma levels of catecholamines were neuropharmacoligically examined using urethaneanestetized rats.Results obtained are as follows. 1) Bombesin i.c.v. dose-dependently (0.3-10 nmole) increased plasma levels of adrenaline (AD) and noradrenaline (NA) [Control: AD; 170 + 28, NA; 429 + 33 pg/ml (n=20).Thirty min after 3 nmole of bombesin: AD; 1145 + 247, NA 719 + 162 pg/ml (n=50)]. Chemical sympathitectomy with 6-hydroxydopamine markedly potentiated this bombesin-induced increase in AD level[Thirty min after 3 nmol of bombesin ; 3600 + 357 pg/ml (n=5)]. Surgical adrenalectomy did not affect the bombesin-induced increase in NA level. 2) Electrical stimu-lation of the preoptic area, central site of action of bombesin, increased both the levels of AD and NA as observed with bombesin. 3) Time of appearance of bombesin-induced increase in the level of AD but not of NA was hastened by pretreatment with an alpha-adrenoceptor blockade, phentolamine (s.c.), but not with a beta-adrenoceptor blockade, propranolol. 4) Intravenous infusion of nicotine increased the levels of both AD and NA in the splanchnicectomized rats. This nicotine-induced increases were not modified by chemical sympathitectomy with 6-hydroxydopamine.These results suggest that sympathetic nervous system has an inhibitory role in the regulatory mechanism of AD secretion. Furthermore, sites of this regulatory mechanism is probably resides in the brain but not in the peripheral target organ, adrenal glands.