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

脑室内(I.C.V.)的影响1)血管紧张素II(AII)可引起动脉压(AP)升高，心率(HR)和肾交感神经活动(RSNA)降低。在去窦主动脉神经(SAD)大鼠，RSNA的抑制反应持续存在。去双侧肾神经后，侧脑室注射AII所致的利钠反应明显减弱。由于RSNA的激活增加了肾小管钠的吸收，这一发现提示中枢AII通过RSNA促进肾脏钠的排泄。2)心房利钠多肽(ANP)对静息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。心钠素不影响AII诱导的HR和RSNA反应。3)ET-3可引起AP升高，HR和RSNA降低。ET-3有时会产生潜伏期为10-15分钟的桶旋转。4)白介素I(IL-1)是一种主要由巨噬细胞产生的细胞因子，具有中枢性作用，如发热和ACTH释放。IL-1在免疫系统和中枢神经系统相互作用中可能起关键作用的自主神经系统的作用尚未很好地阐明。IL-1使AP、HR和RSNA升高，体温升高。这些反应可被消炎痛完全消除。IL-1还可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.