前列腺素E2和前列腺素f2α对大鼠尿钾激肽排泄的影响。

H R Croxatto, R Arriagada, M Rojas, J Roblero, R Rosas
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引用次数: 0

摘要

1. 在正常水合大鼠中,每2小时(3次)皮下注射5微克/100克体重的前列腺素F2alpha (PGF2alpha)可显著增加尿钾激肽活性,并在第一次注射后8小时内增加钠、钾和水的排泄。在中度高水合的大鼠中,用0.5%的NaCl溶液负荷2.5%的体重,PGF2alpha在钾激肽活性和电解质排泄方面产生了类似的变化。2. 在正常水合大鼠中,在相同的条件和剂量下,前列腺素E2 (PGE2)对钾激肽活性没有影响,显示出减少钾和水排泄的趋势。3.5、12.5和25微克/100克体重剂量的PGE2,给药剂量为2.5%和0.5% NaCl和5%自来水/100克体重,1小时后,注射后120分钟收集的尿液中钾激肽激酶活性显著增加。在最高剂量下,钾和水的排泄明显减少。4. PGF2alpha对过水合大鼠的钾激肽活性没有影响,但在最高剂量下,钠排泄量增加,钾排泄量减少。5. PGE2和PGF2alpha的不同作用可能是与钾化钾素-激肽系统相关的调节机制的一部分,钾化钾素-激肽系统有助于维持细胞外液稳态。
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Effects of prostaglandin E2 and prostaglandin F2alpha upon urinary kallikrein excretion in rats.

1. In normally hydrated rats prostaglandin F2alpha (PGF2alpha) in doses of 5 microgram/100 g body weight given subcutaneously every 2 h (three times) induced a significant increase in urinary kallikrein activity, and in sodium, potassium and water excretion for 8 h after the first injection. In moderately hyperhydrated rats loaded 2.5% of body wt. with 0.5% NaCl solution, PGF2alpha produced similar changes in kallikrein activity and electrolyte excretion. 2. In normally hydrated rats prostaglandin E2 (PGE2) in the same conditions and doses as in 1 had no effect on kallikrein activity, showing a tendency to decrease potassium and water excretion. 3. PGE2 in doses of 5, 12.5 and 25 microgram/100 g body wt. in overhydrated rats given 2.5% and 0.5% NaCl and 5% of tap water/100 g body wt. 1 h later, significantly increased kallikrein activity in the urine collected for 120 min after the injections. A significant decrease in potassium and water excretion was observed with the highest dose. 4. PGF2alpha, had no effect on kallikrein activity in overhydrated rats, but an increase in sodium and a decrease in potassium excretion was seen at the highest dose. 5. The different actions of PGE2 and PGF2alpha may be part of a regulatory mechanism associated with the kallikrein-kinin system which contributes maintainance of extracellular fluid homeostasis.

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Proceedings of the Fifth Meeting of the International Society of Hypertension, Paris, 12-14 June 1978. Brain catecholamines and catecholamine-synthesizing enzymes in renovascular hypertension in the rat. Enhanced hypothalamic noradrenaline biosynthesis in Goldblatt I renovascular hypertension. Definitive evidence for renin in rat brain by affinity chromatographic separation from protease. Renal release of active and inactive renin in essential and renovascular hypertension.
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