Attenuated baroreflex control of sympathetic nerve activity in obese Zucker rats by central mechanisms
Attenuated baroreflex control of sympathetic nerve activity in obese Zucker rats by central mechanisms
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DOI：
10.1113/jphysiol.2009.186387
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发表时间：
2010-05-01
影响因子：
5.5
通讯作者：
Schreihofer, Ann M.
中科院分区：
文献类型：
--
作者：
Huber, Domitila A.;Schreihofer, Ann M.
与瘦 Zucker 大鼠 (LZR) 相比，成年肥胖 Zucker 大鼠 (OZR) 对动脉压 (AP) 诱发变化的交感神经反应减少。这项研究检验了 OZR 中交感压力感受性反射的减弱是否可能是由于感觉或中枢机制的改变所致。与乌拉坦麻醉下年龄匹配的 LZR 相比，OZR 的基线内脏交感神经活动 (SNA) 和平均 AP (MAP) 有所升高 (P < 0.05)。在用阿托品和普萘洛尔治疗的大鼠中，通过输注去氧肾上腺素或硝普钠（60-90 秒内+/- 60 mmHg）来改变 AP，同时测量主动脉降压神经活动 (ADNA)，以消除心率的变化。尽管高血压 OZR 中的基线 ADNA 较高，但 OZR 和 LZR 中 MAP 和 ADNA 之间的关系相当。相比之下，与 LZR 相比，ADN 传入纤维的电刺激（5 s 序列、2 ms 脉冲、4 V、0.5-48 Hz）在 OZR 中产生的 SNA 和 MAP 降低幅度要小得多（P < 0.05）。在阻断α-肾上腺素能受体以防止交感神经介导的抑制反应后，OZRs 对 ADN 刺激的交感神经反应仍然减少。此外，与 LZR 相比，电刺激或用苯基双胍（1、2、4 和 8 μg，静脉注射）刺激迷走神经传入神经对 OZR 中的 SNA 产生较小的抑制（P < 0.05）。这些数据表明，交感压力感受性反射减弱是 OZR 中枢机制改变的结果，而不是主动脉压力感受器对 AP 反应性的缺陷。此外，OZR 中 SNA 调节的中枢缺陷延伸到由迷走传入神经引发的其他交感抑制反射。
Adult obese Zucker rats (OZRs) have reduced sympathetic responses to evoked changes in arterial pressure (AP) compared to lean Zucker rats (LZRs). This study examined whether attenuated sympathetic baroreflexes in OZRs may be due to altered sensory or central mechanisms. The OZRs had elevated baseline splanchnic sympathetic nerve activity (SNA) and mean AP (MAP) compared to age-matched LZRs under urethane anaesthesia (P < 0.05). Aortic depressor nerve activity (ADNA) was measured while AP was altered by infusions of phenylephrine or nitroprusside (+/- 60 mmHg over 60-90 s) in rats treated with atropine and propranolol to eliminate changes in heart rate. Although baseline ADNA was higher in the hypertensive OZRs, the relationship between MAP and ADNA was comparable in OZRs and LZRs. In contrast, electrical stimulation of the ADN afferent fibres (5 s train, 2 ms pulses, 4 V, 0.5-48 Hz) produced dramatically smaller reductions in SNA and MAP in OZRs compared to LZRs (P < 0.05). After blockade of alpha-adrenergic receptors to prevent sympathetically mediated depressor responses, OZRs still had reduced sympathetic responses to stimulation of the ADN. In addition, stimulation of vagal afferent nerves electrically or with phenylbiguanide (1, 2, 4 and 8 mu g, i.v.) produced smaller inhibitions of SNA in OZRs compared with LZRs (P < 0.05). These data suggest that attenuated sympathetic baroreflexes are the result of altered central mechanisms in OZRs, and not deficits in the responsiveness of aortic baroreceptors to AP. Furthermore, central deficits in the regulation of SNA in OZRs extend to other sympathoinhibitory reflexes initiated by vagal afferent nerves.