Regulatory Mechanism of Polarized Membrane Transport by Glucocorticoid in Renal Proximal Tubule Cells: Involvement of [Ca2+]i

Journal of Veterinary Medical Science

Ho Jae HAN²  Dae Hoon KIM²  Young Soon LEE¹  Il Suk YANG¹  Jang Hern LEE¹  Soo Hyun PARK² 

[1] College of Veterinary Medicine, Seoul National University, Suwon, 440-744 Korea;Department of Veterinary Physiology, College of Veterinary Medicine, Hormone Research Center, Chonnam National University, Kwangju, 500-757, Korea

关键词: Ca2+/calmodulin;    dexamethasone;    kidney;    Na-Pi cotransporter;   

DOI  :  10.1292/jvms.61.1197

学科分类：兽医学

来源: Japanese Society of Veterinary Science

【 摘 要 】

References(34)Cited-By(2)We examined the effect of glucocorticoids on brush border membrane transporters and, furthermore, the involvement of Ca2+ in its action in the primary cultured rabbit renal proximal tubule cells (PTCs). Dexamethasone (DEX, 10-9 M) decreased Pi uptake by 17%; whereas DEX affected neither α-methyl-glucopyranoside (α-MG) uptake nor Na+ uptake. The DEX-induced inhibition of Pi uptake was due to a decrease of Vmax. In contrast, other steroid hormones such as progesterone, testosterone, and 17β-estradiol (10-9 M) did not induce inhibition of Pi uptake. In order to examine the involvement of Ca2+ in DEX-induced inhibition of Pi uptake, PTCs were treated with A 23187 (10-6 M, Ca2+ ionophore). A 23187 also inhibited Pi uptake, mimicking DEX action in Pi uptake. Treatments with W-7 (10-4 M, calmodulin dependent kinase inhibitor), KN-62 (10-6 M, Ca2+/calmodulin-dependent protein kinase II inhibitor), and BAPTA/AM (10-6 M) or TMB-8 (10-4 M) (intracellular Ca2+ mobilization blockers) blocked the DEX-induced inhibition of Pi uptake. However, nifedifine, methoxyverapamil (10-6 M, L-type Ca2+ channel blockers), and EGTA (1 mM, extracellular Ca2+ chelator) did not block it. In conclusion, DEX inhibited Pi uptake via, in part, Ca2+/calmodulin pathway mediated by intracellular Ca2+ mobilization in the PTCs.

【 授权许可】

Unknown