Suppr超能文献

体位性心动过速综合征(POTS)患者血浆血管紧张素II水平升高与血流和血容量减少有关。

Increased plasma angiotensin II in postural tachycardia syndrome (POTS) is related to reduced blood flow and blood volume.

作者信息

Stewart Julian M, Glover June L, Medow Marvin S

机构信息

Center for Pediatric Hypotension, New York Medical College, Valhalla, NY 10595, USA.

出版信息

Clin Sci (Lond). 2006 Feb;110(2):255-63. doi: 10.1042/CS20050254.

Abstract

POTS (postural tachycardia syndrome) is associated with low blood volume and reduced renin and aldosterone; however, the role of Ang (angiotensin) II has not been investigated. Previous studies have suggested that a subset of POTS patients with increased vasoconstriction related to decreased bioavailable NO (nitric oxide) have decreased blood volume. Ang II reduces bioavailable NO and is integral to the renin-Ang system. Thus, in the present study, we investigated the relationship between blood volume, Ang II, renin, aldosterone and peripheral blood flow in POTS patients. POTS was diagnosed by 70 degrees upright tilt, and supine calf blood flow, measured by venous occlusion plethysmography, was used to subgroup POTS patients. A total of 23 POTS patients were partitioned; ten with low blood flow, eight with normal flow and five with high flow. There were ten healthy volunteers. Blood volume was measured by dye dilution. All biochemical measurements were performed whilst supine. Blood volume was decreased in low-flow POTS (2.14 +/- 0.12 litres/m2) compared with controls (2.76 +/- 0.20 litres/m2), but not in the other subgroups. PRA (plasma renin activity) was decreased in low-flow POTS compared with controls (0.49 +/- 0.12 compared with 0.90 +/- 0.18 ng of Ang I.ml(-1).h(-1) respectively), whereas plasma Ang II was increased (89 +/- 20 compared with 32 +/- 4 ng/l), but not in the other subgroups. PRA correlated with aldosterone (r = +0.71) in all subjects. PRA correlated negatively with blood volume (r = -0.72) in normal- and high-flow POTS, but positively (r = +0.65) in low-flow POTS. PRA correlated positively with Ang II (r = +0.76) in normal- and high-flow POTS, but negatively (r = -0.83) in low-flow POTS. Blood volume was negatively correlated with Ang II (r = -0.66) in normal- and high-flow POTS and in five low-flow POTS patients. The remaining five low-flow POTS patients had reduced blood volume and increased Ang II which was not correlated with blood volume. The data suggest that plasma Ang II is increased in low-flow POTS patients with hypovolaemia, which may contribute to local blood flow dysregulation and reduced NO bioavailability.

摘要

直立性心动过速综合征(POTS)与血容量降低以及肾素和醛固酮减少有关;然而,血管紧张素(Ang)II的作用尚未得到研究。先前的研究表明,一部分POTS患者因生物可利用的一氧化氮(NO)减少导致血管收缩增加,进而血容量降低。Ang II可降低生物可利用的NO,是肾素-血管紧张素系统的重要组成部分。因此,在本研究中,我们调查了POTS患者的血容量、Ang II、肾素、醛固酮与外周血流之间的关系。通过70度直立倾斜试验诊断POTS,采用静脉阻塞体积描记法测量仰卧位小腿血流,以此对POTS患者进行亚组划分。共纳入23例POTS患者,其中10例血流较低,8例血流正常,5例血流较高。另有10名健康志愿者。通过染料稀释法测量血容量。所有生化指标均在仰卧位时检测。与对照组(2.76±0.20升/平方米)相比,低血流POTS患者的血容量降低(2.14±0.12升/平方米),但其他亚组未见此现象。与对照组相比(分别为0.49±0.12与0.90±0.18纳克血管紧张素I·毫升-1·小时-1),低血流POTS患者的血浆肾素活性(PRA)降低,而血浆Ang II升高(分别为89±20与32±4纳克/升),但其他亚组未见此现象。所有受试者中,PRA与醛固酮呈正相关(r = +0.71)。在正常血流和高血流POTS患者中,PRA与血容量呈负相关(r = -0.72),而在低血流POTS患者中呈正相关(r = +0.65)。在正常血流和高血流POTS患者中,PRA与Ang II呈正相关(r = +0.76),而在低血流POTS患者中呈负相关(r = -0.83)。在正常血流和高血流POTS患者以及5例低血流POTS患者中,血容量与Ang II呈负相关(r = -0.66)。其余5例低血流POTS患者血容量降低,Ang II升高,且二者无相关性。数据表明,低血流且血容量不足的POTS患者血浆Ang II升高,这可能导致局部血流调节异常以及NO生物利用度降低。

相似文献

2
Persistent splanchnic hyperemia during upright tilt in postural tachycardia syndrome.
Am J Physiol Heart Circ Physiol. 2006 Feb;290(2):H665-73. doi: 10.1152/ajpheart.00784.2005. Epub 2005 Sep 2.
3
Regional blood volume and peripheral blood flow in postural tachycardia syndrome.
Am J Physiol Heart Circ Physiol. 2004 Sep;287(3):H1319-27. doi: 10.1152/ajpheart.00086.2004. Epub 2004 Apr 29.
5
Abnormalities of angiotensin regulation in postural tachycardia syndrome.
Heart Rhythm. 2011 Mar;8(3):422-8. doi: 10.1016/j.hrthm.2010.11.009. Epub 2011 Jan 22.
6
Distinct neurohumoral biomarker profiles in children with hemodynamically defined orthostatic intolerance may predict treatment options.
Am J Physiol Heart Circ Physiol. 2016 Feb 1;310(3):H416-25. doi: 10.1152/ajpheart.00583.2015. Epub 2015 Nov 25.
7
Renin-aldosterone paradox and perturbed blood volume regulation underlying postural tachycardia syndrome.
Circulation. 2005 Apr 5;111(13):1574-82. doi: 10.1161/01.CIR.0000160356.97313.5D. Epub 2005 Mar 21.
8
Altered systemic hemodynamic and baroreflex response to angiotensin II in postural tachycardia syndrome.
Circ Arrhythm Electrophysiol. 2012 Feb;5(1):173-80. doi: 10.1161/CIRCEP.111.965343. Epub 2012 Jan 13.
9
The hemodynamic and neurohumoral phenotype of postural tachycardia syndrome.
Neurology. 2007 Aug 21;69(8):790-8. doi: 10.1212/01.wnl.0000267663.05398.40.
10
Pooling in chronic orthostatic intolerance: arterial vasoconstrictive but not venous compliance defects.
Circulation. 2002 May 14;105(19):2274-81. doi: 10.1161/01.cir.0000016348.55378.c4.

引用本文的文献

1
Blood volume deficit in postural orthostatic tachycardia syndrome assessed by semiautomated carbon monoxide rebreathing.
Clin Auton Res. 2025 Apr;35(2):267-276. doi: 10.1007/s10286-024-01091-8. Epub 2024 Nov 30.
2
Navigating Complexity in Postural Orthostatic Tachycardia Syndrome.
Biomedicines. 2024 Aug 20;12(8):1911. doi: 10.3390/biomedicines12081911.
4
Evidence for Impaired Renin Activity in Postural Orthostatic Tachycardia Syndrome.
J Clin Med. 2023 Jul 13;12(14):4660. doi: 10.3390/jcm12144660.
5
Adrenal gland response to adrenocorticotropic hormone is intact in patients with postural orthostatic tachycardia syndrome.
Auton Neurosci. 2023 Sep;248:103105. doi: 10.1016/j.autneu.2023.103105. Epub 2023 Jun 24.
6
COVID-19 Induced Postural Orthostatic Tachycardia Syndrome (POTS): A Review.
Cureus. 2023 Mar 31;15(3):e36955. doi: 10.7759/cureus.36955. eCollection 2023 Mar.
8
Effect of High Dietary Sodium Intake in Patients With Postural Tachycardia Syndrome.
J Am Coll Cardiol. 2021 May 4;77(17):2174-2184. doi: 10.1016/j.jacc.2021.03.005.
9
Impaired Endothelial Function in Patients With Postural Tachycardia Syndrome.
Hypertension. 2021 Mar 3;77(3):1001-1009. doi: 10.1161/HYPERTENSIONAHA.120.16238. Epub 2021 Jan 25.

本文引用的文献

1
Researches on the Circulation Time and on the Influences which affect it.
J Physiol. 1897 Nov 20;22(3):159-83. doi: 10.1113/jphysiol.1897.sp000684.
2
Decreased microvascular nitric oxide-dependent vasodilation in postural tachycardia syndrome.
Circulation. 2005 Oct 25;112(17):2611-8. doi: 10.1161/CIRCULATIONAHA.104.526764. Epub 2005 Oct 17.
3
Renin-aldosterone paradox and perturbed blood volume regulation underlying postural tachycardia syndrome.
Circulation. 2005 Apr 5;111(13):1574-82. doi: 10.1161/01.CIR.0000160356.97313.5D. Epub 2005 Mar 21.
4
Regional blood volume and peripheral blood flow in postural tachycardia syndrome.
Am J Physiol Heart Circ Physiol. 2004 Sep;287(3):H1319-27. doi: 10.1152/ajpheart.00086.2004. Epub 2004 Apr 29.
5
Control of aldosterone secretion: a model for convergence in cellular signaling pathways.
Physiol Rev. 2004 Apr;84(2):489-539. doi: 10.1152/physrev.00030.2003.
6
Alterations in sympathetic ganglionic transmission in response to angiotensin II in (mRen2)27 transgenic rats.
Hypertension. 2004 Feb;43(2):270-5. doi: 10.1161/01.HYP.0000112422.81661.f3. Epub 2004 Jan 19.
7
Methods for the investigation of peripheral blood flow.
Br Med Bull. 1963 May;19:101-9. doi: 10.1093/oxfordjournals.bmb.a070026.
8
Local vascular responses affecting blood flow in postural tachycardia syndrome.
Am J Physiol Heart Circ Physiol. 2003 Dec;285(6):H2749-56. doi: 10.1152/ajpheart.00429.2003. Epub 2003 Aug 14.
9
Interactions of angiotensin II with NAD(P)H oxidase, oxidant stress and cardiovascular disease.
J Renin Angiotensin Aldosterone Syst. 2003 Jun;4(2):51-61. doi: 10.3317/jraas.2003.014.
10
Microvascular filtration is increased in postural tachycardia syndrome.
Circulation. 2003 Jun 10;107(22):2816-22. doi: 10.1161/01.CIR.0000070951.93566.FC. Epub 2003 May 19.

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验