The Hypertension & Vascular Research Center, Wake Forest Univ. School of Medicine, Medical Center Boulevard, Winston-Salem, NC 27157-1032, USA.
Am J Physiol Heart Circ Physiol. 2011 Jun;300(6):H2206-13. doi: 10.1152/ajpheart.01263.2010. Epub 2011 Apr 1.
The renal medulla plays an important role in cardiovascular regulation, through interactions with the autonomic nervous system. Hydronephrosis is characterized by substantial loss of renal medullary tissue. However, whether alterations in autonomic control of the heart are observed in this condition is unknown. Thus we assessed resting hemodynamics and baroreflex sensitivity (BRS) for control of heart rate in urethane/chloralose-anesthetized Sprague-Dawley rats with normal or hydronephrotic kidneys. While resting arterial pressure was similar, heart rate was higher in rats with hydronephrosis (290 ± 12 normal vs. 344 ± 11 mild/moderate vs. 355 ± 13 beats/min severe; P < 0.05). The evoked BRS to increases, but not decreases, in pressure was lower in hydronephrotic rats (1.06 ± 0.06 normal vs. 0.72 ± 0.10 mild/moderate vs. 0.63 ± 0.07 ms/mmHg severe; P < 0.05). Spectral analysis methods confirmed reduced parasympathetic function in hydronephrosis, with no differences in measures of indirect sympathetic activity among conditions. As a secondary aim, we investigated whether autonomic dysfunction in hydronephrosis is associated with activation of the renin-angiotensin system (RAS). There were no differences in circulating angiotensin peptides among conditions, suggesting that the impaired autonomic function in hydronephrosis is independent of peripheral RAS activation. A possible site for angiotensin II-mediated BRS impairment is the solitary tract nucleus (NTS). In normal and mild/moderate hydronephrotic rats, NTS administration of the angiotensin II type 1 receptor antagonist candesartan significantly improved the BRS, suggesting that angiotensin II provides tonic suppression to the baroreflex. In contrast, angiotensin II blockade produced no significant effect in severe hydronephrosis, indicating that at least within the NTS baroreflex suppression in these animals is independent of angiotensin II.
肾髓质在心血管调节中起着重要作用，通过与自主神经系统的相互作用。肾积水的特征是大量肾髓质组织丧失。然而，在这种情况下，自主控制心脏的变化是否被观察到尚不清楚。因此，我们评估了在正常或肾积水的乌拉坦/氯醛糖麻醉的 Sprague-Dawley 大鼠中，静息血液动力学和压力反射敏感性（BRS）对心率的控制。虽然静息动脉压相似，但肾积水大鼠的心率更高（290±12 正常比 344±11 轻度/中度比 355±13 次/分重度；P<0.05）。肾积水大鼠对压力增加而非降低的诱发 BRS 较低（1.06±0.06 正常比 0.72±0.10 轻度/中度比 0.63±0.07 ms/mmHg 重度；P<0.05）。 谱分析方法证实肾积水时副交感神经功能降低，但在条件之间间接交感神经活动的测量没有差异。作为次要目标，我们研究了肾积水自主神经功能障碍是否与肾素-血管紧张素系统（RAS）的激活有关。在条件之间，循环血管紧张素肽没有差异，表明肾积水自主神经功能障碍与外周 RAS 激活无关。血管紧张素 II 介导的 BRS 损害的可能部位是孤束核（NTS）。在正常和轻度/中度肾积水大鼠中，NTS 给予血管紧张素 II 型 1 受体拮抗剂坎地沙坦可显著改善 BRS，表明血管紧张素 II 对压力反射提供紧张抑制。相反，血管紧张素 II 阻断在严重肾积水大鼠中没有产生显著效果，表明至少在 NTS 中，这些动物的血压反射抑制独立于血管紧张素 II。
