Churchill P C, Churchill M C, McDonald F D
J Pharmacol Exp Ther. 1986 Feb;236(2):331-3.
It has been shown previously that ouabain, vanadate, angiotensin II and 0 and 60 mM KCl media have Ca-dependent inhibitory effects on renin secretory rates of rat renal cortical slices. In the present experiments, replacing extracellular CaCl2 with SrCl2 did not impair the inhibitory effects on renin secretion in this preparation. Moreover, methoxyverapamil antagonized the inhibitory effect of K-depolarization. The inhibitory effects and methoxyverapamil-induced antagonism of the inhibitory effect of K-depolarization, suggest that increased intracellular Sr++ can lead to inhibition of renin secretion, perhaps directly or perhaps by causing the release or mobilization of Ca++ from intracellular sites of binding or sequestration. These results add to the growing evidence that Ca++ plays an inhibitory second messenger role in the renin secretory process.
先前的研究表明，哇巴因、钒酸盐、血管紧张素 II 以及 0 和 60 mM 的 KCl 培养基对大鼠肾皮质切片的肾素分泌率具有钙依赖性抑制作用。在本实验中，用 SrCl2 替代细胞外 CaCl2 并不会损害该制剂对肾素分泌的抑制作用。此外，甲氧基维拉帕米可拮抗 K+ 去极化的抑制作用。K+ 去极化的抑制作用以及甲氧基维拉帕米对其抑制作用的拮抗表明，细胞内 Sr++ 增加可导致肾素分泌受到抑制，这可能是直接作用，也可能是通过促使 Ca++ 从细胞内结合或储存部位释放或动员所致。这些结果进一步证明了 Ca++ 在肾素分泌过程中起着抑制性第二信使的作用。
