Biphasic effect of extracellular [K] on isoproterenol-stimulated renin secretion from rat kidney slices.

Biphasic effect of extracellular [K] on isoproterenol-stimulated renin secretion from rat kidney slices.
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细胞外 [K] 对异丙肾上腺素刺激的大鼠肾切片肾素分泌的双相作用。

DOI:
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发表时间:
1980
影响因子:
3.5
通讯作者:
M. Churchill
M. Churchill
中科院分区:
医学2区
文献类型:
--
作者:
P. Churchill;M. Churchill

文献摘要

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已知细胞外K浓度[K]的较大变化,无论是从正常的方向还是从正常的方向,都会导致细胞的去极化,并且已经表明去极化抑制肾小球细胞分泌肾素。在本实验中,大鼠肾切片的肾素分泌作为[K]的函数进行了检查。增加[k](从4-45或60 mM)抑制基础和异丙肾上腺素刺激的肾素分泌,独立于[Na],[Cl]和渗透压的变化。在4,45和60 mM K,细胞外[Na]的减少也抑制分泌;异丙肾上腺素的联合作用。钙拮抗剂D-600拮抗高[K]的抑制作用,恢复基础和异丙肾上腺素刺激的分泌率到正常值。降低[K](从2.5-1.0 mM)也抑制基础和异丙肾上腺素刺激的分泌,这种作用不拮抗D-600。根据D-600的已知作用和目前的观察结果,我们认为去极化本身并不抑制肾素分泌,但细胞内[Ca]的增加(在高[K]存在下由去极化诱导的Ca内流或在低[K]存在下由Na-Ca交换速率的变化引起)拮抗基础和异丙肾上腺素刺激的肾素分泌。
It is known that large changes in extracellular K concentration [K], in either direction from normal, lead to depolarization of the cell and it has been suggested that depolarization inhibits the secretion of renin from juxtaglomerular cells. In the present experiments, renin secretion of rat kidney slices was examined as a function of [K]. Increases in [k] (from 4-45 or to 60mM) inhibited basal and isoproterenol-stimulated renin secretion, independently of changes in [Na], [Cl] and osmolality. At 4, 45 and 60 mM K, reductions in extracellular [Na] also inhibited secretion; the combined effect of isoproterenol. The Ca antagonist D-600 antagonized the inhibitory effects of high [K], restoring both the basal and the isoproterenol-stimulated secretory rates to normal values. Decreasing [K] (from 2.5-1.0 mM) also inhibited basal and isoproterenol-stimulated secretion, and this effect was not antagonized by D-600. On the basis of the known actions of D-600 and the present observations, it is suggested that depolarization per se does not inhibit renin secretion but that increases in intracellular [Ca] (resulting from depolarization-induced Ca influx in the presence of high [K] or from changes in the rate of Na-Ca exchange in the presence of low [K]) antagonize both basal and isoproterenol-stimulated renin secretion.