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首页> 外文期刊>American Journal of Physiology >Evidence for a role of protein kinase C-alpha in urine concentration.
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Evidence for a role of protein kinase C-alpha in urine concentration.

机译：蛋白激酶C-α在尿液浓度中的作用的证据。

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摘要

In mouse kidney, the conventional protein kinase C (PKC) isoenzyme alpha is expressed in glomeruli, the cortical collecting duct (intercalated cells only), and medullary collecting duct. To get insights on its function, PKC-alpha knockout (-/-) and wild-type (+/+) mice were studied. When provided free access to water, PKC-alpha -/- mice showed approximately 50% greater urine flow rate and lower urinary osmolality in 24-h metabolic cage experiments despite a greater urinary vasopressin-to-creatinine ratio vs. PKC-alpha +/+ mice. Renal albumin excretion was not different. Clearance experiments under inactin/ketamine anesthesia revealed a modestly reduced glomerular filtration rate and showed a reduced absolute and fractional renal fluid reabsorption in PKC-alpha -/- mice. The sodium-restricting response to a low-sodium diet was unaffected in PKC-alpha -/- mice. Urinary osmolality was reduced to similar hypotonic levels in PKC-alpha -/- and +/+ mice during acute oral water loading or application of the vasopressin V(2)-receptor antagonist SR-121463. In comparison, the lower urinary osmolality observed in PKC-alpha -/- mice vs. wild-type mice under basal conditions persisted during water restriction for 36 h. In conclusion, PKC-alpha appears not to play a major role in renal sodium reabsorption but, consistent with its expression in the medullary collecting duct, contributes to urinary concentration in mice. Considering that PKC-beta I and -beta II are coexpressed with PKC-alpha in mouse medullary collecting duct, the present results indicate that conventional PKC isoenzymes cannot fully compensate for each other.
机译：在小鼠肾脏中，传统的蛋白激酶C（PKC）同功酶α在肾小球，皮质收集管（仅插入细胞）和髓样收​​集管中表达。为了了解其功能，研究了PKC-α基因敲除（-/-）和野生型（+ / +）小鼠。当提供自由饮水时，尽管尿中加压素与肌酐的比例相对于PKC-α+ /较高，但PKC-α-/-小鼠在24小时代谢笼实验中显示出大约50％的尿流率增加和尿渗透压降低。 +老鼠。肾白蛋白排泄无异。在inactin /氯胺酮麻醉下的清除实验显示，在PKC-α-/-小鼠中，肾小球滤过率适度降低，肾液的绝对和分数再吸收降低。对低钠饮食的限钠反应在PKC-α-/-小鼠中不受影响。在急性口服水负荷或加压素V（2）-受体拮抗剂SR-121463的应用过程中，PKC-alpha-/-和+ / +小鼠的尿渗透压降低至相似的低渗水平。相比之下，在基础条件下，PKC-α-/-小鼠相对于野生型小鼠在基本水分限制下持续36 h观察到较低的尿渗透压。总之，PKC-α似乎在肾钠重吸收中没有起主要作用，但与它在髓样收集管中的表达一致，有助于小鼠中的尿液浓度。考虑到PKC-βI和-βII与PKC-α在小鼠骨髓收集管中共表达，目前的结果表明常规PKC同工酶不能充分补偿彼此。

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