心房钠尿多肽对麻醉大鼠血压和肾神经传出放电的影响

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

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。

The effects of atriopeptin Ⅲ(AP Ⅲ)on the arterial pressure(AP),heart rate(HR)and renal sympathetic nerve activity(RSNA)were investigated in anesthe-tized rats.The results were as follows:(1)In intact rats(n=12),following intra-venous injection of AP Ⅲ(50 μg/kg),systolic arterial pressure(SAP)decreased by23.0±1.66 mmHg(M±SE,P<0.001),HR decreased by 9±3.5 beats/min(P<0.05),and RSNA decreased by 4.89±2.95%(P>0.05).After vagotomy,the de-crease in SAP following iv.AP Ⅲ showed no significant difference with that of in-tact rats.HR showed no change,while there was a small increase in RSNA(P>0.05);(2)In the intact vagi but sinoaortic denervated rats(n=7),intravenous APⅢ decreased SAP by 27.4±3.25 mmHg(P<0.001),HR by 13±3.1 beats/min(P<0.01),and RSNA by 11.67±1.95%(P<0.001).After vagotomy,the decreasein SAP following iv.AP Ⅲ was attenuated,HR showed no significant change,butthere was a small but significant increase in RSNA(P<0.05);(3)Following intra-venous injection of nitroprusside,SAP decreased significantly.Such a hypotensiveeffect was associated with an increase in RSNA in either the intact or the vagotomizedrats.The results indicate that(1)the hypotensive effect of AP Ⅲ was mediated part-ly by vagi;(2)in the sinoaortic denervated rats AP Ⅲ could reflexly inhibit RSNAby activation of vagal afferent fibers.