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β-肾上腺素能受体阻断前后分级肾神经刺激期间的肾去甲肾上腺素溢出

Renal norepinephrine overflow during graded renal nerve stimulation before and after beta-adrenoceptor blockade.

作者信息

Chen Y H, Blair M L, Izzo J L

出版信息

J Auton Nerv Syst. 1984 Nov;11(3):285-95. doi: 10.1016/0165-1838(84)90042-0.

DOI:10.1016/0165-1838(84)90042-0
PMID:6096433
Abstract

These experiments were designed to determine if renal venous norepinephrine (NE) overflow provides a valid index of renal sympathetic nerve activity. In addition, we evaluated the effect of beta-adrenoceptor blockade on renal NE overflow during graded renal nerve stimulation in order to examine the possibility that presynaptic beta-adrenoceptors facilitate neuronal release of NE in the kidney. In 6 pentobarbital-anesthetized dogs, the renal nerves were transected to remove tonic nerve activity and the distal ends were electrically stimulated (8-25 V, 0.5 ms) over the range of 0.3-5.0 Hz for consecutive 4-min periods. NE overflow rate was calculated as the product of the veno-arterial NE concentration difference and renal plasma flow. Control values of NE overflow (-8.7 +/- 1.8 ng/min) demonstrated net clearance of NE from the renal circulation. NE overflow rate rose to -3.1 +/- 2.2, 1.0 +/- 4.0, and 33.2 +/- 15.4 ng/min at 0.3, 0.6, and 1.2 Hz stimulation, respectively, with no accompanying change in renal blood flow. At 2.4 and 5.0 Hz, renal blood flow decreased by 21 +/- 4% and 37 +/- 3%, but there was no further increase in NE overflow rate (38.8 +/- 9.4 and 27.8 +/- 6.5 ng/min). Propranolol (0.5-1.0 mg . kg-1 plus 0.4-0.5 mg . kg-1 i.v., n = 4) did not alter the effect of nerve stimulation on either NE overflow or renal blood flow. Thus we were unable to demonstrate the presence of functional renal presynaptic beta-adrenoceptors. Further, our data indicate that renal norepinephrine overflow rate is not always a reliable index of renal nerve activity, since NE overflow was not proportional to renal nerve stimulation rate at frequencies high enough to cause vasoconstriction.

摘要

这些实验旨在确定肾静脉去甲肾上腺素(NE)溢出是否能提供肾交感神经活动的有效指标。此外,我们评估了β-肾上腺素能受体阻断对分级肾神经刺激期间肾NE溢出的影响,以研究突触前β-肾上腺素能受体促进肾脏中NE神经元释放的可能性。在6只戊巴比妥麻醉的犬中,切断肾神经以消除紧张性神经活动,并在连续4分钟内以0.3 - 5.0Hz的频率对远端进行电刺激(8 - 25V,0.5ms)。NE溢出率通过静脉-动脉NE浓度差与肾血浆流量的乘积来计算。NE溢出的对照值(-8.7±1.8ng/min)表明肾循环中NE有净清除。在0.3、0.6和1.2Hz刺激时,NE溢出率分别升至-3.1±2.2、1.0±4.0和33.2±15.4ng/min,肾血流量无伴随变化。在2.4和5.0Hz时,肾血流量分别下降21±4%和37±3%,但NE溢出率无进一步增加(38.8±9.4和27.8±6.5ng/min)。普萘洛尔(0.5 - 1.0mg·kg-1静脉注射加0.4 - 0.5mg·kg-1静脉注射,n = 4)未改变神经刺激对NE溢出或肾血流量的影响。因此,我们无法证明功能性肾突触前β-肾上腺素能受体的存在。此外,我们的数据表明,肾去甲肾上腺素溢出率并不总是肾神经活动的可靠指标,因为在足以引起血管收缩的频率下,NE溢出与肾神经刺激率不成比例。

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引用本文的文献

1
[Modulation of renal transmitter release by presynaptic receptors].[突触前受体对肾递质释放的调节作用]
Klin Wochenschr. 1989 Sep 1;67(17):865-9. doi: 10.1007/BF01717341.