Splanchnic sympathetic nerves in the development of mild DOCA-salt hypertension
Splanchnic sympathetic nerves in the development of mild DOCA-salt hypertension
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DOI：
10.1152/ajpheart.00086.2011
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发表时间：
2011-11-01
影响因子：
4.8
通讯作者：
Fink, Gregory D.
中科院分区：
文献类型：
--
作者：
Kandlikar, Sachin S.;Fink, Gregory D.
广东港康里卡SS。内脏交感神经在轻度doca -盐高血压发生中的作用。[J]中国生物医学工程学报，2016,31(2):555 - 557。首次发表于2011年9月2日；doi: 10.1152 / ajpheart.00086.2011。-我们以前报道过轻度醋酸脱氧皮质酮（DOCA）盐高血压是在没有全身性交感神经兴奋的情况下发生的。然而，交感神经系统活动（SNA）是区域异质性的，因此我们开始研究交感神经对特定区域的作用。我们对这种可能性的第一项研究显示，肾神经对高血压的发展没有贡献。内脏交感神经参与血压调节，因为内脏去神经支配能有效降低高血压患者的血压。在这里，我们检验了内脏SNA有助于轻度doca盐高血压发展的假设。一组大鼠通过腹腔神经节切除术（CGX）实现内脏去神经控制，另一组进行假手术（sham - gx）。在双肾完好的大鼠中，经DOCA （50 mg/kg）治疗后，CGX大鼠的血压增幅与SHAM-GX大鼠相比显著减弱（DOCA治疗后第28天，15.6 +/- 2.2 vs. 25.6 +/- 2.2 mmHg）。在其他大鼠中，测量全身去甲肾上腺素（NE）溢出，以确定CGX是否通过降低整体SNA来减轻高血压的发展，在SHAM-GX和CGX大鼠之间没有发现差异。在第三组中，非肝脏内脏NE外溢被测量为内脏SNA的一个指标，但在高血压发展过程中，SHAM（非DOCA治疗）和DOCA大鼠之间没有差异。在最后一组中，CGX有效地消除了非肝脏内脏NE外溢。这些数据表明，完整的内脏神经支配是轻度doca -盐高血压发展所必需的，而不是增加内脏SNA或NE释放。在doca盐治疗期间内脏血管对NE的反应性增加是一种可能的解释。
Kandlikar SS, Fink GD. Splanchnic sympathetic nerves in the development of mild DOCA-salt hypertension. Am J Physiol Heart Circ Physiol 301: H1965-H1973, 2011. First published September 2, 2011; doi:10.1152/ajpheart.00086.2011.-We previously reported that mild deoxycorticosterone acetate (DOCA)-salt hypertension develops in the absence of generalized sympathoexcitation. However, sympathetic nervous system activity (SNA) is regionally heterogeneous, so we began to investigate the role of sympathetic nerves to specific regions. Our first study on that possibility revealed no contribution of renal nerves to hypertension development. The splanchnic sympathetic nerves are implicated in blood pressure (BP) regulation because splanchnic denervation effectively lowers BP in human hypertension. Here we tested the hypothesis that splanchnic SNA contributes to the development of mild DOCA-salt hypertension. Splanchnic denervation was achieved by celiac ganglionectomy (CGX) in one group of rats while another group underwent sham surgery (SHAM-GX). After DOCA treatment (50 mg/kg) in rats with both kidneys intact, CGX rats exhibited a significantly attenuated increase in BP compared with SHAM-GX rats (15.6 +/- 2.2 vs. 25.6 +/- 2.2 mmHg, day 28 after DOCA treatment). In other rats, whole body norepinephrine (NE) spillover, measured to determine if CGX attenuated hypertension development by reducing global SNA, was not found to be different between SHAM-GX and CGX rats. In a third group, nonhepatic splanchnic NE spillover was measured as an index of splanchnic SNA, but this was not different between SHAM (non-DOCA-treated) and DOCA rats during hypertension development. In a final group, CGX effectively abolished nonhepatic splanchnic NE spillover. These data suggest that an intact splanchnic innervation is necessary for mild DOCA-salt hypertension development but not increased splanchnic SNA or NE release. Increased splanchnic vascular reactivity to NE during DOCA-salt treatment is one possible explanation.