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钾、钠、灌注压及异丙肾上腺素对急性钙缺乏诱导的肾素释放的影响。

Influence of potassium, sodium, perfusion pressure, and isoprenaline on renin release induced by acute calcium deprivation.

作者信息

Fray J C, Park C S

出版信息

J Physiol. 1979 Jul;292:363-72. doi: 10.1113/jphysiol.1979.sp012856.

Abstract
  1. These studies were conducted in isolated perfused rat kidneys to determine the influence of perfusion pressure, isoprenaline, K, and Na on renin release stimulated by acute Ca deprivation.2. Removing Ca from the perfusion medium for 10 min stimulated renin release and reintroducing Ca returned it toward control values.3. Lowering concentration of Ca in the perfusion medium from 5 to 0 mM increased the effectiveness of low perfusion pressure (50 mmHg) and isoprenaline (2.43 muM) in stimulating renin release.4. At higher perfusion pressure (150 mmHg), renin release was inhibited in perfusion medium containing 2.5 mM-Ca but not in medium containing no Ca. In fact, high perfusion pressure stimulated renin release when the perfusion medium was without Ca.5. Raising concentration of K in the perfusion medium partially inhibited the renin release induced by Ca deprivation. Adding 5 mM-EGTA to Ca-deprived medium stimulated a greater rate of renin release than that of Ca-deprived medium alone. This greater renin release was also partially inhibited by raising K concentration in the perfusion medium.6. Lowering concentration of Na in the perfusion medium from 145 to 25 mM partially inhibited the renin release induced by Ca deprivation in the presence of low perfusion pressure or isoprenaline.7. These findings support the hypothesis that a decreased concentration of Ca in the cytoplasm of the juxtaglomerular cell stimulates renin release and increased Ca inhibits renin release. The sequence of events which leads to changes in cytoplasmic Ca might depend on the concentration of Ca in the perfusion medium, the renal perfusion pressure, the membrane potential of the juxtaglomerular cells, and Ca-Na exchange mechanisms.
摘要
  1. 这些研究在离体灌注的大鼠肾脏中进行,以确定灌注压力、异丙肾上腺素、钾和钠对急性钙缺乏刺激的肾素释放的影响。

  2. 从灌注介质中去除钙10分钟会刺激肾素释放,重新引入钙会使其恢复到对照值。

  3. 将灌注介质中的钙浓度从5 mM降至0 mM,可增强低灌注压力(50 mmHg)和异丙肾上腺素(2.43 μM)刺激肾素释放的效果。

  4. 在较高灌注压力(150 mmHg)下,含2.5 mM钙的灌注介质中肾素释放受到抑制,但不含钙的介质中则未受抑制。实际上,当灌注介质无钙时,高灌注压力会刺激肾素释放。

  5. 提高灌注介质中钾的浓度可部分抑制钙缺乏诱导的肾素释放。向缺钙介质中添加5 mM乙二醇双四乙酸(EGTA)比单独的缺钙介质刺激更高的肾素释放速率。这种更高的肾素释放也会因提高灌注介质中钾的浓度而部分受到抑制。

  6. 在低灌注压力或异丙肾上腺素存在的情况下,将灌注介质中的钠浓度从145 mM降至25 mM可部分抑制钙缺乏诱导的肾素释放。

  7. 这些发现支持以下假说:球旁细胞质中钙浓度降低会刺激肾素释放,而钙浓度升高则会抑制肾素释放。导致细胞质钙变化的事件顺序可能取决于灌注介质中的钙浓度、肾灌注压力、球旁细胞的膜电位以及钙 - 钠交换机制。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8c2e/1280863/4b02e0b7f265/jphysiol00869-0377-a.jpg

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