Kinin effects on electrogenic ion transport in primary cultures of pig renal papillary collecting tubule cells.
Kinin effects on electrogenic ion transport in primary cultures of pig renal papillary collecting tubule cells.
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激肽对猪肾乳头集合管细胞原代培养物中生电离子转运的影响。
DOI：
10.1152/ajprenal.1985.249.3.f439
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发表时间：
1985
期刊：
影响因子：
--
通讯作者：
MacVinish,L
中科院分区：
文献类型：
--
作者：
Cuthbert,AW;George,AM;MacVinish,L
猪肾乳头状集合管（RPCT）细胞的汇合单层在胶原蛋白包被的Millipore过滤器上形成。它们被夹在Ussing型室中，用于测量短路电流（SCC）。单层细胞低电位（0.1 mV），基底侧为阳性。在短路条件下，有小的内向电流流过。在添加一些药剂后，SCC增加。与SCC变化相关的受体的分布如下：对于激肽（例如，赖氨酰-缓激肽），它们存在于组织的两侧，而精氨酸加压素和去甲肾上腺素的那些仅存在于基底外侧。上皮细胞对加入到组织顶面或基底面的PGE 2有反应;应用于一侧阻止了对侧的反应。这些组织也对佛司可林（一种腺苷酸环化酶的激活剂）产生反应，其持续的内向电流对呋塞米敏感。在暴露于8-溴腺苷-3 '，5'-环一磷酸（BrcAMP）后记录到类似的持续内向电流。通过用吲哚美辛或吡罗昔康抑制脂肪酸环氧合酶或用不渗透性离子代替氯离子来减弱对激肽的反应。如果SCC首先增加与毛喉素，BrcAMP，或去甲肾上腺素，激肽对SCC的影响被取消或逆转。它的结论是，激肽可以引起氯化物分泌的RPCT单层，可能通过前列腺素或腺苷酸环化酶的机制。不排除通过首先提高组织cAMP水平而暴露的激肽的次级效应。
Confluent monolayers of pig renal papillary collecting tubule (RPCT) cells were formed on Millipore filters coated with collagen. They were clamped in Ussing-type chambers and used to measure short-circuit current (SCC). The monolayers had low potentials (0.1 mV) with the basolateral side positive. Small inward currents flowed under short-circuit conditions. Increases in SCC were obtained following addition of a number of agents. Receptors associated with SCC changes were disposed as follows: for kinins (e.g., lysyl-bradykinin) they were present on both sides of the tissue, while those for arginine vasopressin and norepinephrine were present on the basolateral side only. Epithelia responded to PGE2 added to the apical or basolateral face of the tissue; application to one side prevented the response from the contralateral side. The tissues also responded to forskolin, an activator of adenylate cyclase, with a sustained inward current that was sensitive to furosemide. Similar sustained inward currents were recorded following exposure to 8-bromoadenosine-3',5'-cyclic monophosphate (BrcAMP). Responses to kinins were attenuated by inhibition of fatty acid cyclooxygenase with either indomethacin or piroxicam or by replacing chloride with impermeant ions. If the SCC was first increased with forskolin, BrcAMP, or norepinephrine, the kinin effects on SCC were either abolished or reversed. It is concluded that kinin can cause chloride secretion in RPCT monolayers, possibly via a prostaglandin or a prostaglandin-adenylate cyclase mechanism. Secondary effects of kinin, exposed by first raising tissue cAMP levels, are not precluded.