心房钠尿多肽对麻醉大鼠血压和肾神经传出放电的影响

本实验观察了心房肽Ⅱ(Atriopeptin Ⅱ,APⅡ)对麻醉大鼠血压(AP)、心率(HR)和肾交感神经传出放电(RSNA)的影响,并与硝普钠对 AP 和 RSNA 的影响作比较。结果如下:(1)缓冲神经完整和迷走神经完整条件下(n=12)静脉注射 APⅡ(50μg/kg)后,动脉收缩压(SAP)降低23.0±1.66 mmHg(Μ±SE,p<0.001),HR 减慢9±3.5b/min(p<0.05),RSNA 降低4.89±2.95%(P>0.05)。迷走神经切断后,静脉注射 APⅡ引起的~⊿SAP 虽有所减小,但与切断迷走神经前的反应比较,无统计学意义,HR 减慢不再出现,而 RSNA 则有所增加;(2)缓冲神经切断和迷走神经完整条件下(n=7),静脉注射 APⅡ时 SAP 降低27.4±3.25mmHg(P<0.001),HR 减慢13±3.1b/min(P<0.01),RSNA 降低11.67±1.95%(P<0.001)。切断迷走神经后,静脉注射 APⅡ引起的 SAP 降低程度有明显減小(P<0.01),HR减慢不再出现,RSNA 则反而增加(3)无论在迷走神经完整还是切断条件下,静脉注射硝普钠(n=6) SAP 均明显降低,同时伴有 RSNA 的反射性增加。以上结果表明:APⅡ的降压效应,部分是通过迷走神经传入纤维;在切断缓冲神经条件下,APⅡ可经由迷走神经传入纤维的激活而反射地抑制 RSNA。

EFFECTS OF ATRIAL NATRIURETIC POLYPEPTIDE ON ARTERIAL PRESSURE AND RENAL SYMPATHETIC NERVE ACTIVITY IN ANESTHETIZED RATS

The effects of atriopeptin III (AP III) on the arterial pressure (AP), heart rate (HR) and renal sympathetic nerve activity (RSNA) were investigated in anesthetized rats. The results were as follows: (1) In intact rats (n = 12), following intravenous injection of AP III (50 micrograms/kg), systolic arterial pressure (SAP) decreased by 23.0 +/- 1.66 mmHg (M +/- SE, P less than 0.001), HR decreased by 9 +/- 3.5 beats/min (P less than 0.05), and RSNA decreased by 4.89 +/- 2.95% (P greater than 0.05). After vagotomy, the decrease in SAP following iv. AP III showed no significant difference with that of intact rats. HR showed no change, while there was a small increase in RSNA (P greater than 0.05); (2) In the intact vagi but sinoaortic denervated rats (n = 7), intravenous AP III decreased SAP by 27.4 +/- 3.25 mmHg (P less than 0.001), HR by 13 +/- 3.1 beats/min (P less than 0.01), and RSNA by 11.67 +/- 1.95% (P less than 0.001). After vagotomy, the decrease in SAP following i.v. AP III was attenuated, HR showed no significant change, but there was a small but significant increase in RSNA (P less than 0.05); (3) Following intravenous injection of nitroprusside, SAP decreased significantly. Such a hypotensive effect was associated with an increase in RSNA in either the intact or the vagotomized rats. The results indicate that (1) the hypotensive effect of AP III was mediated partly by vagi; (2) in the sinoaortic denervated rats AP III could reflexly inhibit RSNA by activation of vagal afferent fibers.