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KMID : 0811719990030010083
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Korean Journal of Physiology & Pharmacology
1999 Volume.3 No. 1 p.83 ~ p.91
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The Roles of Arachidonic Acid and Calcium in the Angiotensin Ⅱ-induced Inhibition of Na+ Uptake in Renal Proximal Tubule Cells
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Soo Hyun Park
Hyun Joo Koh/Yeun Hee Lee/Chang Ho Son/Min Kyoung Park/Young Jae Lee/Ho Jae Han
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Abstract
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Angiotensin II (ANG II) has a biphasic effect on Na+ transport in proximal tubule: low doses of ANG II increase the Na+ transport, whereas high doses of ANG II inhibit it. However, the mechanisms of high dose ANG II-induced inhibition on Na+ uptake are poorly understood. Thus the aim of the present study was to investigate signal transduction pathways involved in the ANG II-induced inhibition of Na+ uptake in the primary cultured rabbit renal proximal tubule cells (PTCs) in hormonally defined serum-free medium. ANG II (10?9M)?induced inhibition of Na+ uptake was blocked by losartan (10?8M,AT1antagonist), but not by PD123319 (10?8M,AT2antagonist) (P<0.05). ANG II-induced inhibition of Na+ uptake was also completely abolished by neomycin (10?4M, PLC inhibitor), W-7 (10?4M, calmodulin antagonist), and AACOCF3(10?6M,PLA2inhibitor) (P<0.05). ANG II significantly increased [3H]arachidonic acid (AA) release compared to control. The ANG II-induced [3H]AA release was blocked by losartan, AACOCF3, neomycin, and W-7, but not by PD123319. ANG II-induced [3H]AA release in the presence of extracellular Ca2+ was greater than in Ca2+?free medium, and it was partially blocked by TMB-8 (10?4M, intracelluar Ca2+ mobilization blocker). However, in the absence of extracellular Ca2+, it was completely blocked by TMB-8. In addition, econazole (10?6M, cytochrome P-450 monooxygenase inhibitor) and indomethacin (10?6M, cyclooxygenase inhibitor) blocked ANG II-induced inhibition of Na+ uptake, but NGDA (10?6M, lipoxygenase inhibitor) did not affect it. In conclusion, PLA2?mediated AA release is involved in ANG II-induced inhibition of Na+ uptake and is modulated by [Ca2+]i in the PTCs.
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KEYWORD
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Angiotensin Ⅱ, Arachidonic acid, Ca2, , Kidney, Na, transport,
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