Activation of vagal depressor reflexes by atriopeptins inhibits renal sympathetic nerve activity.
Activation of vagal depressor reflexes by atriopeptins inhibits renal sympathetic nerve activity.
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心房肽激活迷走神经抑制反射抑制肾交感神经活动。
DOI：
10.1152/ajpheart.1986.251.6.h1252
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发表时间：
1986
期刊：
影响因子：
--
通讯作者：
Brody,MJ
中科院分区：
文献类型：
--
作者：
Thoren,P;Mark,AL;Morgan,DA;O'Neill,TP;Needleman,P;Brody,MJ
心房利钠因子降低动脉压，但降压反应不伴有预期的反射性心动过速。反射性心动过速的缺失可能反映了心房钠素（心房肽）对迷走神经传入的心脏感觉受体的刺激作用。为了验证AP通过激活迷走神经传入神经抑制交感神经活动的假设，我们测量了麻醉后的Sprague-Dawley大鼠在完整状态下、经窦主动脉去神经支配后、经窦主动脉去神经支配加双侧迷走神经切断后，注射APII和APIII时肾交感神经活动（SNA）、心率和动脉压的变化。在完整的麻醉大鼠中，APIII（50微克/千克）降低了平均动脉压[-31 +/- 8 (SE) mmHg]，而没有预期的肾SNA和心率反射性增加。相比之下，输注硝普钠的剂量与平均动脉压（-29 +/- 9 mmHg）相似，可引起肾SNA（+38 +/- 8%）和心率（+17 +/- 5次/分钟）的显著增加。在窦主动脉去神经的大鼠中，APIII诱导平均动脉压更大的下降（-44 +/- 8 mmHg）。这种降压反应与肾SNA降低（-26 +/- 2%）相关，双侧迷走神经切开术可消除这种降低。阿托品没有减轻APIII患者肾SNA的下降。我们得出结论，APII和APIII增加迷走神经传入活动，从而抑制肾SNA和心率的增加，这可能是由动脉压下降引起的。我们推测这一作用可能促进了APs的肾血管扩张和利钠作用。
Atrial natriuretic factor decreases arterial pressure but the hypotensive response is not accompanied by the expected reflex tachycardia. The absence of reflex tachycardia might reflect a stimulating effect of atrial natriuretic factor [atriopeptins (AP)] on cardiac-sensory receptors with vagal afferents. To test the hypothesis that AP inhibit sympathetic nerve activity by activating vagal afferents we measured changes in renal sympathetic nerve activity (SNA), heart rate, and arterial pressure during injection of APII and APIII in anesthetized Sprague-Dawley rats in the intact state, after sinoaortic denervation, and after sinoaortic denervation plus bilateral vagotomy. In intact, anesthetized rats APIII (50 micrograms/kg) lowered mean arterial pressure [-31 +/- 8 (SE) mmHg] without the expected reflex increase in renal SNA and heart rate. In contrast, infusion of sodium nitroprusside in a dose that produced a similar decrease in mean arterial pressure (-29 +/- 9 mmHg) evoked a significant increase in renal SNA (+38 +/- 8%) and heart rate (+17 +/- 5 beats/min). In rats with sinoaortic denervation, APIII induced a greater fall in mean arterial pressure (-44 +/- 8 mmHg). This hypotensive response was associated with a decrease in renal SNA (-26 +/- 2%) that was abolished by bilateral vagotomy. Atropine did not attenuate the decrease in renal SNA with APIII. We conclude that APII and APIII increase the activity of vagal afferents and thereby inhibit the increases in renal SNA and heart rate, which would be expected to result from the fall in arterial pressure. We speculate that this action might facilitate reflexly the renal vasodilator and natriuretic actions of APs.