Brain peptides : central regulation of the cardiovascular, renal and autonomic nervous functions in conscious rats

脑室内（i。C.（五）1）血管紧张素II（AII）引起动脉血压（AP）升高、心率（HR）和肾交感神经活动（RSNA）降低。RSNA的抑制反应在去窦房结神经（SAD）大鼠中持续存在。i.诱导的利钠反应。C. v.双侧肾去神经后，AII明显减弱。由于RSNA的激活增加肾小管钠吸收，这一发现表明，中央AII通过RSNA对肾钠排泄具有促进作用。与正常对照组相比，SAD大鼠的饮水量明显增加，提示压力感受器参与了SAD大鼠饮水行为的控制。2）心钠素（ANP）对大鼠静息AP、HR、RSNA和肾血流量无明显影响。然而，预先给予ANP可减弱AII诱导的升压反应。内皮素-3（ET-3）可引起AP升高，HR和RSNA降低。ET-3有时产生潜伏期为10-15 min的桶形旋转，此时HR和RSNA显著而持久地增加。4）白细胞介素I（IL-1）是一种主要由巨噬细胞产生的细胞因子，具有发热和ACTH释放等中枢作用。IL-1对自主神经系统的影响可能在免疫系统和中枢神经系统之间的相互作用中起关键作用，但尚未得到很好的阐明。IL-1增加AP，HR和RSNA，随后体温升高。吲哚美辛可完全消除上述反应。IL-1还增加血浆去甲肾上腺素和ACTH浓度。

Effects of intracerebroventricular (i. c. v.) administration of peptides on cardiovascular function and renal sympathetic nerve activity (RSNA) were examined in conscious rats.1)Angiotensin II (AII) elicited an increase in arterial blood pressure (AP) and decreases in heart rate (HR) and RSNA. The inhibitory response of RSNA persisted in sinoaorticdenervated (SAD) rats. Natriuretic response induced by i. c. v. AII was greatly attenuated after bilateral renal denervation. Since activation of RSNA increases tubular sodium absorption, the finding suggests that central AII has facilitatory effect on renal sodium excretion through the RSNA. Water intake induced by All was enhanced in SAD rats, compared to that in intact rats, suggesting involvement of baroreceptors in control of drinking behaviour.2)Atrial natriuretic polypeptide (ANP) had no significant effects on resting AP, HR, RSNA and renal blood flow. Prior administration of ANP however, attenuated AII-induced pressor response. HR and RSNA responses induced by AII were not affected by the ANP.3)Endothelin-3 (ET-3) elicited an increase in AP and decreases in HR and RSNA. ET-3 sometimes produced a barrel rotation with a latency of 10-15 min. At the time, prominent and long-lasting increases in HR and RSNA occurred.4)Interleukin I (IL-1), a cytokine essentially produced by macrophage, has central actions such as fever and ACTH release. Effects of IL-1 on autonomic nervous system, which may play a critical role in the interaction between the immune system and the central nervous system, has not well elucidated. IL-1 increased AP, HR and RSNA followed by an increase in body temperature. The responses were completely abolished by indomethacin. IL-1 also increased plasm noradrenaline and ACTH concentrations.