Thorén P, Mark A L, Morgan D A, O'Neill T P, Needleman P, Brody M J
Am J Physiol. 1986 Dec;251(6 Pt 2):H1252-9. doi: 10.1152/ajpheart.1986.251.6.H1252.
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.
心房利钠因子可降低动脉血压，但这种降压反应并未伴随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利钠因子[心房肽（AP）]对具有迷走神经传入纤维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纤维来抑制交感神经活动这一假说，我们在完整状态下、去窦主动脉神经支配后以及去窦主动脉神经支配加双侧迷走神经切断术后，对麻醉的Sprague-Dawley大鼠注射APII和APIII期间，测量了肾交感神经活动（SNA）、心率和动脉血压的变化。在完整的麻醉大鼠中，APIII（50微克/千克）可降低平均动脉压[-31±8（SE）毫米汞柱]，而肾SNA和心率并未出现预期的反射性增加。相比之下，输注能使平均动脉压产生类似降低幅度（-29±9毫米汞柱）的硝普钠，可引起肾SNA显著增加（+38±8%）和心率增加（+17±5次/分钟）。在去窦主动脉神经支配的大鼠中，APIII导致平均动脉压下降幅度更大（-44±8毫米汞柱）。这种降压反应与肾SNA降低（-26±2%）有关，而双侧迷走神经切断术可消除这种降低。阿托品并未减弱APIII引起的肾SNA降低。我们得出结论，APII和APIII可增加迷走神经传入纤维的活动，从而抑制动脉血压下降所预期的肾SNA和心率增加。我们推测，这一作用可能会反射性地促进AP的肾血管舒张和利钠作用。
