Orce G G, Castillo G A, Margolius H S
Am J Physiol. 1980 Nov;239(5):F459-65. doi: 10.1152/ajprenal.1980.239.5.F459.
Aprotinin, a reversible inhibitor, and D-Phe-Phe-Arg-chloromethyl ketone (DPPA), an irreversible inhibitor of mammalian glandular kallikreins, decreased short-circuit current (SCC) in the isolated toad urinary bladder. Both were more potent and rapidly acting on the mucosal than serosal surface. The maximal inhibition in basal SCC was 29% for aprotinin and 41% for DPPA at concentrations of 7.0 X 10(-6) and 1.0 X 10(-5) M, respectively. SCC inhibition with mucosal aprotinin was reversed by rinsing, whereas inhibition with mucosal DPPA was not reversible. The presence of either agent in the mucosal bath inhibited the SCC increase to serosal vasopressin, but neither modified this response when present in the serosal bath. Neither agent affected basal or vasopressin-stimulated osmotic water permeability. Aprotinin did not prevent aldosterone-induced increases in SCC. Soybean trypsin inhibitor, an inhibitor of plasma but not glandular kallikrein, did not affect SCC. We postulate that these inhibitors of mammalian glandular kallikreins act upon some accessible serine proteinase(s) to reduce short-circuit current. This protein(s) might be an amphibian homologue of mammalian renal kallikrein.
抑肽酶是一种可逆性抑制剂，而D - 苯丙氨酸 - 苯丙氨酸 - 精氨酸 - 氯甲基酮（DPPA）是哺乳动物腺体激肽释放酶的不可逆性抑制剂，它们均可降低离体蟾蜍膀胱的短路电流（SCC）。二者对黏膜表面的作用均比浆膜表面更强且起效更快。在浓度分别为7.0×10⁻⁶和1.0×10⁻⁵ M时，抑肽酶对基础SCC的最大抑制率为29%，DPPA为41%。用黏膜抑肽酶处理后，通过冲洗可使SCC抑制作用逆转，而用黏膜DPPA处理后的抑制作用则不可逆转。在黏膜浴中加入任何一种试剂均可抑制浆膜血管加压素引起的SCC增加，但当它们存在于浆膜浴中时，均不改变这种反应。两种试剂均不影响基础或血管加压素刺激的渗透水通透性。抑肽酶不能阻止醛固酮诱导的SCC增加。大豆胰蛋白酶抑制剂是血浆而非腺体激肽释放酶的抑制剂，对SCC无影响。我们推测，这些哺乳动物腺体激肽释放酶的抑制剂作用于某些可及的丝氨酸蛋白酶，从而降低短路电流。这种蛋白酶可能是哺乳动物肾激肽释放酶的两栖类同源物。
