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血管加压素与人类高血压

Vasopresin and human hypertension.

作者信息

Del Bo Alberto

机构信息

Centro di Fisiologia Clinica e Ipertensione, Università degli Studi di Milano, Ospedale Maggiore, Milan, Italy.

出版信息

Cell Mol Neurobiol. 2003 Oct;23(4-5):617-24. doi: 10.1023/a:1025032431763.

Abstract
  1. Two clinical studies are reported which investigate: (1) the regulation of vasopressin release in moderate hypertensive subjects not under treatment compared to normotensives and, (2) the effects of antihypertensive treatment on vasopressin and on its osmoregulation in moderate hypertensives. 2. In the first study two stimuli facilitating vasopressin release (active upright position and hypertonic saline infusion) and a stimulus inhibiting vasopressin release (hypotonic saline infusion) have been applied to 13 moderate essential hypertensives and 8 control normotensives. In the second study, limited to hypertensives, the effects on plasma vasopressin and other plasma and urine variables, of either acute (by clonidine, n = 6 or by sodium nitroprusside, n = 6) or chronic (antihypertensive treatment for 1 month, n = 8) blood pressure lowering, before and after the i.v. administration of a hypertonic NaCl solution, were investigated. 3. Baseline plasma vasopressin was not different in hypertensive and in normotensive subjects. Upright posture and hypertonic challenge augmented, while hypotonic saline reduced plasma vasopressin levels with no difference between the two groups. Acute, but not chronic, lowering of blood pressure increased plasma vasopressin from 1.6 +/- 0.63 to 3.4 +/- 0.7 pg/mL (p < 0.05); administration of hypertonic saline further increased vasopressin to 10.8 +/- 2.22 (p < 0.01) in the acute and to 6.0 +/- 1.03 pg/mL (p < 0.01) in the chronic study. 4. No significant alterations of the regulation of vasopressin have been found in moderate, uncomplicated hypertension. Moreover, acute lowering of blood pressure facilitated the release of vasopressin and its osmoregulation while a chronic antihypertensive treatment did not interfere with a normal control of vasopressin secretion.
摘要
  1. 报告了两项临床研究,其旨在调查:(1)与血压正常者相比,未经治疗的中度高血压患者中血管加压素释放的调节情况;(2)降压治疗对中度高血压患者血管加压素及其渗透调节的影响。2. 在第一项研究中,对13名中度原发性高血压患者和8名对照血压正常者施加了两种促进血管加压素释放的刺激(主动直立位和高渗盐水输注)以及一种抑制血管加压素释放的刺激(低渗盐水输注)。在第二项研究中,仅限于高血压患者,研究了静脉注射高渗氯化钠溶液前后,急性(通过可乐定,n = 6或通过硝普钠,n = 6)或慢性(降压治疗1个月,n = 8)降低血压对血浆血管加压素以及其他血浆和尿液变量的影响。3. 高血压患者和血压正常者的基线血浆血管加压素无差异。直立姿势和高渗刺激会增加血浆血管加压素水平,而低渗盐水会降低血浆血管加压素水平,两组之间无差异。急性而非慢性降低血压会使血浆血管加压素从1.6±0.63增加至3.4±0.7 pg/mL(p < 0.05);在急性研究中,给予高渗盐水会使血管加压素进一步增加至10.8±2.22(p < 0.01),在慢性研究中增加至6.0±1.03 pg/mL(p < 0.01)。4. 在中度、无并发症的高血压中未发现血管加压素调节有明显改变。此外,急性降低血压促进了血管加压素的释放及其渗透调节,而慢性降压治疗并未干扰血管加压素分泌的正常控制。

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1
Vasopresin and human hypertension.血管加压素与人类高血压
Cell Mol Neurobiol. 2003 Oct;23(4-5):617-24. doi: 10.1023/a:1025032431763.

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