神经激肽A在大鼠输精管中诱导的高效钙离子动员。

Efficient Ca2+ mobilization induced by neurokinin A in rat vas deferens.

作者信息

Nagata K, Saito H, Matsuki N

机构信息

Department of Chemical Pharmacology, Faculty of Pharmaceutical Sciences, University of Tokyo, Japan.

出版信息

Eur J Pharmacol. 1991 Nov 12;204(3):295-300. doi: 10.1016/0014-2999(91)90855-k.

DOI:10.1016/0014-2999(91)90855-k

PMID:1663458

Abstract

Although both neurokinin A (NKA) and norepinephrine (NE) induced similar maximal contractions in the epididymal and the prostatic site of vas deferens, NKA affected sensitivity more potently than did NE in both sites. The NKA-induced contractions were more strongly inhibited by nicardipine, a dihydropyridine Ca2+ entry blocker, or by elimination of extracellular Ca2+ (Cao2+) in both sites. However, ryanodine, which interferes with the release of intracellular Ca2+ (Cai2+), abolished the contractions caused by NKA in the prostatic site whereas it had no effect in the epididymal site. These results suggest that NKA-induced contraction utilizes both Cai2+ and Cao2+ in the prostatic site but mobilizes only Cao2+ in the epididymal site. Cai2+ concentration [( Ca2+]i) was measured directly with a Ca(2+)-sensitive fluorescent dye, fura-2. In the epididymal site NKA induced contractions with smaller increase in [Ca2+]i compared to that necessary for NE-induced contractions. These results suggest that NKA utilizes Ca2+ more efficiently than does NE and plays a role as a neuromodulator in rat vas deferens.

摘要

尽管神经激肽A（NKA）和去甲肾上腺素（NE）在输精管的附睾段和前列腺段诱导出相似的最大收缩，但在这两个部位，NKA对敏感性的影响比NE更强。在这两个部位，NKA诱导的收缩均被二氢吡啶类钙通道阻滞剂尼卡地平或通过去除细胞外Ca²⁺（Caₒ²⁺）更强烈地抑制。然而，干扰细胞内Ca²⁺（Caᵢ²⁺）释放的ryanodine消除了前列腺段由NKA引起的收缩，而在附睾段则无作用。这些结果表明，NKA诱导的收缩在前列腺段利用了Caᵢ²⁺和Caₒ²⁺两者，但在附睾段仅动员了Caₒ²⁺。用Ca²⁺敏感荧光染料fura - 2直接测量Ca²⁺浓度[Ca²⁺]ᵢ。在附睾段，与NE诱导收缩所需的[Ca²⁺]ᵢ增加相比，NKA诱导收缩时[Ca²⁺]ᵢ的增加较小。这些结果表明，NKA比NE更有效地利用Ca²⁺，并在大鼠输精管中作为神经调节剂发挥作用。