Stretch receptor control of renin release in perfused rat kidney: effect of high perfusate potassium.
Stretch receptor control of renin release in perfused rat kidney: effect of high perfusate potassium.
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灌注大鼠肾脏中肾素释放的牵张受体控制：高灌注液钾的作用。
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发表时间：
1978
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影响因子：
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通讯作者：
J. Fray
中科院分区：
文献类型：
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作者：
J. Fray
1.这些研究在离体灌注大鼠肾脏中进行，以确定高灌注液K对低灌注压、肾血管收缩和异丙肾上腺素诱导的肾素释放的影响，并确定K诱导的抑制程度是否与肾血管舒张和高灌注压下观察到的抑制程度相同。2.将灌注液K浓度从4.2 mM升高至56 mM抑制了基础肾素释放，56 mM-K抑制了低灌注压（50 mmHg）或苯肾上腺素（0.83 μ m）诱导的肾素释放。3.异丙肾上腺素（0.79微米）引起的显着增加，肾素释放，但高灌注K，普萘洛尔（0.28毫米），罂粟碱（0.39毫米），或高灌注压（150毫米汞柱）抑制这种效果。4.它的结论是，高灌流液K有一个强大的抑制作用，肾性低血压，血管收缩，异丙肾上腺素输注引起的肾素释放，这种效果可能是模仿高灌注压或肾血管舒张。提出了一种机制，使这些信号可能抑制肾素释放的肾小球颗粒细胞去极化。
1. These studies were conducted in the isolated perfused rat kidney to determine the effect of high perfusate K on the renin release induced by low perfusion pressure, renal vasoconstriction and isoprenaline, and to determine whether the magnitude of the K‐induced inhibition equalled that observed with renal vasodilation and high perfusion pressure. 2. Raising perfusate K concentration from 4.2 to 56 mM suppressed basal renin release, and the 56 mM‐K inhibited the renin release induced by low perfusion pressure (50 mmHg) or phenylephrine (0.83 micrometers). 3. Isoprenaline (0.79 micrometers) induced a marked increase in renin release; but high perfusate K, propranolol (0.28 mM), papaverine (0.39 mM), or high perfusion pressure (150 mmHg) inhibited this effect. 4. It is concluded that high perfusate K has a powerful inhibitory effect on the renin release induced by renal hypotension, vasoconstriction, and isoprenaline infusion, and that this effect may be mimicked by high perfusion pressure or renal vasodilation. A mechanism is proposed whereby these signals may inhibit renin release by depolarizing the juxtaglomerular granular cells.