The sympathetic nervous system and hypertension - Recent developments
The sympathetic nervous system and hypertension - Recent developments
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DOI：
10.1161/01.hyp.0000113047.47711.fa
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发表时间：
2004-02-01
期刊：
影响因子：
8.3
通讯作者：
DiBona, GF
中科院分区：
文献类型：
--
作者：
DiBona, GF
颈动脉压力感受器导致动脉压立即持续7天升高，并伴随心率和血浆肾素活性增加以及尿钠排泄减少，反映了心脏和肾脏交感神经活动的持续增加（几乎没有重置）。 9 当血管紧张素 II 输注 5 天产生高血压时，受神经支配的肾脏的尿钠排泄量与去神经支配的肾脏相比增加。 10 有人认为这是由动脉压力反射引起的 RSNA 持续减少（几乎没有重置）引起的，并且通过窦主动脉去神经减少受神经支配的肾脏尿钠排泄的发现证实了这一点。动脉压力反射能够产生更长时间持续的 RSNA 降低（几乎没有或没有重置），这一事实通过以下事实得到证明：在血管紧张素的 10 天加压输注过程中，受神经支配的肾脏的尿钠排泄量仍然增加。 11 总的来说，这些研究提供了间接证据，证明 RSNA 因动脉压力感受器卸载或加载而发生的变化可以持续很长一段时间。这支持了以下观点：RSNA 的动脉压力感受反射控制以及整体肾脏排泄功能对动脉压的长期调节有重要贡献。对注射血管紧张素 II 7 天的清醒兔子进行的 RSNA 直接记录明确支持了这一观点。 12 动脉压持续增加 18 mmHg，伴随着 RSNA 持续下降，在血管紧张素 II 输注第 2 天和第 7 天分别减少 56% 和 50%。此外，在血管紧张素 II 输注的第 2 天或第 7 天，动脉压和 RSNA 之间的动脉压力反射关系没有重置（没有转变为较低或较高的动脉压）。与基础状态相比，动脉压力反射的范围减小，增益没有改变，并且静息点从曲线的最陡部分移至曲线的较低平台部分。因此，在血管紧张素 II 输注期间，动脉压从静息点进一步升高不会导致 RSNA 进一步降低。总体而言，RSNA 的抑制似乎通过增加肾脏排泄功能并将压力尿钠排泄关系转变为较低动脉压而在降低高血压程度方面发挥补偿作用。这些结果清楚地表明，动脉压力反射在动脉压的长期变化过程中调节RSNA，并表明动脉压力反射对RSNA的控制以及整体肾脏排泄功能对于动脉压的短期和长期调节至关重要。因此，RSNA 的动脉压力反射控制和整体肾脏排泄功能的缺陷可能导致动脉压调节的改变。支持这一观点的是大鼠的研究结果，即动脉压力感受器去神经支配（1）损害低钠饮食摄入和高钠饮食摄入期间建立钠平衡的能力，并且表现出慢性窦主动脉去神经支配；（2）导致高钠饮食摄入期间动脉压升高，并与肾钠潴留增加相关。 13 动脉压力反射介导的 RSNA 抑制似乎也存在于其他形式的高血压中。在患有窦主动脉去神经支配的兔子中，用 L-NAME 慢性一氧化氮合酶阻断未能产生慢性持续的动脉压升高。 14 这些结果证实，动脉压力反射在长期...
carotid baroreceptors led to an immediate and sustained 7-day increase in arterial pressure in association with increases in heart rate and plasma renin activity and decreases in urinary sodium excretion, reflecting sustained increases in sympathetic nerve activity (with little to no resetting) to heart and kidneys. 9 When hypertension was produced by 5 days of angiotensin II infusion, urinary sodium excretion from the innervated kidney increased compared with that from the denervated kidney. 10 The suggestion that this was caused by an arterial baroreflex-induced sustained decrease in RSNA (with little to no resetting) and was confirmed by the finding that sinoaortic denervation decreased urinary sodium excretion from the innervated kidney. The ability of the arterial baroreflex to produce even longer sustained decreases in RSNA (with little to no resetting) was demonstrated by the fact that urinary sodium excretion from the innervated kidney remained increased throughout a 10-day pressor infusion of angiotensin. 11 Collectively, these studies provided indirect evidence that alterations in RSNA in response to unloading or loading of arterial baroreceptors can be sustained for prolonged periods of time. This supports the suggestion that arterial baroreflex control of RSNA, and thus overall renal excretory function, contribute importantly to the long-term regulation of arterial pressure. Direct recording of RSNA in conscious rabbits infused with angiotensin II for 7 days unambiguously support this view. 12 The sustained increase of 18 mmHg in arterial pressure was accompanied by a sustained decrease in RSNA, which was reduced by 56% and 50% on days 2 and 7 of angiotensin II infusion, respectively. Moreover, the arterial baroreflex relationship between arterial pressure and RSNA was not reset (no shift to either lower or higher arterial pressure) on either day 2 or day 7 of angiotensin II infusion. Compared with the basal state, the range of the arterial baroreflex was reduced, the gain was not changed, and the resting point was moved from the steepest part of the curve to the lower plateau portion of the curve. Thus, during angiotensin II infusion, further increases in arterial pressure from the resting point did not produce further decreases in RSNA. Overall, it appears that suppression of RSNA serves a compensatory role in decreasing the magnitude of the hypertension by increasing renal excretory function and shifting the pressure natriuresis relationship to a lower arterial pressure. These results clearly demonstrate that arterial baroreflexes regulate RSNA during long-term changes in arterial pressure and suggest that arterial baroreflex control of RSNA, and thus overall renal excretory function, is critical in the short-term and long-term regulation of arterial pressure. Thus, defective arterial baroreflex control of RSNA and overall renal excretory function could contribute to altered regulation of arterial pressure. In support of this are the findings in rats that arterial baroreceptor denervation (1) impairs the ability to establish sodium balance during lowsodium dietary intake and high-sodium dietary intake and that chronic sinoaortic denervation is exhibited and (2) leads to the development of increased arterial pressure during highsodium dietary intake in association with increased renal sodium retention. 13It appears that arterial baroreflex-mediated suppression of RSNA is present in other forms of hypertension, also. Chronic nitric oxide synthase blockade with L-NAME in rabbits with sinoaortic denervation failed to produce a chronic sustained increase in arterial pressure. 14 These results confirm that arterial baroreflexes are importantly involved in the long-term …