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

研究了清醒大鼠脑室内注射多肽对心血管功能和肾交感神经活动的影响。1)血管紧张素II （Angiotensin II， AII）引起动脉血压（AP）升高，心率（HR）和RSNA降低。RSNA抑制反应在神经中枢神经支配（SAD）大鼠中持续存在。双侧肾去神经处理后，icv - AII诱导的尿钠反应明显减弱。由于RSNA的激活增加了肾小管钠的吸收，这一发现表明，中央AII通过RSNA对肾钠排泄具有促进作用。与正常大鼠相比，All诱导的饮水量在SAD大鼠中增加，这表明压力感受器参与控制饮酒行为。2)心房钠素多肽（ANP）对静息AP、HR、RSNA及肾血流量无显著影响。然而，先前给予ANP可减弱aii诱导的升压反应。AII诱导的HR和RSNA反应不受anp的影响。3)内皮素-3 （ET-3）引起AP升高，HR和RSNA降低。ET-3有时会产生10-15分钟潜伏期的桶旋转。与此同时，HR和RSNA出现了显著且持久的升高。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的相互作用中起关键作用，但尚未得到很好的阐明。IL-1升高AP、HR和RSNA，随后体温升高。吲哚美辛完全消除了这些反应。IL-1也增加了血浆去甲肾上腺素和ACTH的浓度。

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.