Margolius H S, Halushka P V, Chao J, Miller D H, Cuthbert A W, Spayne J A
Soc Gen Physiol Ser. 1985;39:121-33.
Tissue kallikrein of colon mucosa is synthesized rapidly, and this synthetic process can now be examined in relation to hormonal or dietary manipulations or pathological circumstances that affect intestinal ion transport. Although the identical renal tissue enzyme is known to be enriched in membranes of distal convoluted tubular epithelial cells, the precise localization of the intestinal enzyme is uncertain. An understanding of the intestinal cellular locale of kallikrein will help in defining its local role. That tissue kallikreins can be inhibited by monovalent cations and some drugs (e.g., amiloride) and that kallikrein inhibitors affect cation transport across epithelial surfaces containing such enzymes must be reconciled with the new observations of kinin-induced chloride secretion. Extracellular calcium, eicosanoid synthesis, and cyclic nucleotide production are involved in the secretory response to kinins, although an absolute requirement for intact eicosanoid synthesis may not exist.
结肠黏膜组织激肽释放酶合成迅速,现在可以结合影响肠道离子转运的激素或饮食干预或病理情况来研究这一合成过程。虽然已知相同的肾组织酶在远曲小管上皮细胞膜中富集,但肠道酶的确切定位尚不确定。了解激肽释放酶在肠道细胞中的位置将有助于明确其局部作用。组织激肽释放酶可被单价阳离子和一些药物(如氨氯吡咪)抑制,并且激肽释放酶抑制剂会影响阳离子跨含有此类酶的上皮表面的转运,这必须与激肽诱导的氯离子分泌的新观察结果相协调。细胞外钙、类花生酸合成和环核苷酸生成参与了对激肽的分泌反应,尽管可能并非绝对需要完整的类花生酸合成。