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慢性盐负荷自发性高血压大鼠的血压与肾小管-肾小球反馈机制

Blood pressure and tubuloglomerular feedback mechanism in chronically salt-loaded spontaneously hypertensive rats.

作者信息

Ushiogi Y, Takabatake T, Häberle D A

机构信息

Physiologisches Institut der Universität München, Germany.

出版信息

Kidney Int. 1991 Jun;39(6):1184-92. doi: 10.1038/ki.1991.150.

DOI:10.1038/ki.1991.150
PMID:1895672
Abstract

Experiments were performed to qualitatively characterize the effects of tubuloglomerular feedback (TGF) inhibition by chronic salt loading on salt sensitivity of blood pressure in spontaneously hypertensive rats (SHR). After two weeks of salt loading, systolic blood pressure (SBP) was significantly exacerbated and plasma volume (PV) was expanded in salt-loaded SHR compared with those in control SHR (SBP: 182 +/- 1 vs. 159 +/- 2 mm Hg; PV: 4.38 +/- 0.06 vs. 4.04 +/- 0.03 ml/100 g body wt, respectively). Plasma volume of WKY was also but only transiently expanded by salt loading, whereas plasma volume expansion in SHR had persisted over the entire dietary treatment period. TGF activity was assessed as the maximal reduction of single nephron GFR (SNGFR) on increasing loop of Henle perfusion rate from 0 to 40 nl/min using previously collected tubular fluid from salt-loaded rats (TFs) or control rats (TFc). Maximal TGF response in salt-loaded SHR with TFs was 14.9 +/- 2.9% and 57.8 +/- 2.6% with TFc. In control SHR the responses were 16.9 +/- 2.5% with TFs and 52.7 +/- 2.9% with TFc. In salt-loaded WKY the response with TFs were 3.1 +/- 1.6% and 37.4 +/- 2.8% with TFc. And in control WKY, the response with TFs were 8.2 +/- 1.9% and 40.8 +/- 2.8% with TFc, respectively. These results indicate the TGF resetting in chronically salt-loaded SHR and WKY is caused by the activation of humoral TGF inhibitory factor. The suppression of TGF in SHR was, however, far more variable and, on average, less than in WKY.(ABSTRACT TRUNCATED AT 250 WORDS)

摘要

进行实验以定性表征慢性盐负荷对自发性高血压大鼠(SHR)肾小管球反馈(TGF)的抑制作用对血压盐敏感性的影响。盐负荷两周后,与对照SHR相比,盐负荷SHR的收缩压(SBP)显著升高,血浆容量(PV)增加(SBP:182±1对159±2 mmHg;PV:4.38±0.06对4.04±0.03 ml/100 g体重)。盐负荷使WKY的血浆容量也仅短暂增加,而SHR的血浆容量在整个饮食治疗期间持续增加。使用先前收集的盐负荷大鼠(TFs)或对照大鼠(TFc)的肾小管液,将髓袢灌注速率从0增加到40 nl/min时,单肾单位肾小球滤过率(SNGFR)的最大降低作为TGF活性的评估指标。盐负荷SHR使用TFs时的最大TGF反应为14.9±2.9%,使用TFc时为57.8±2.6%。对照SHR中,使用TFs时的反应为16.9±2.5%,使用TFc时为52.7±2.9%。盐负荷WKY中,使用TFs时的反应为3.1±1.6%,使用TFc时为37.4±2.8%。对照WKY中,使用TFs时的反应分别为8.2±1.9%和40.8±2.8%。这些结果表明,慢性盐负荷的SHR和WKY中TGF的重置是由体液性TGF抑制因子的激活引起的。然而,SHR中TGF的抑制变化更大,平均而言比WKY中的要小。(摘要截断于250字)

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