Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:2.7.11.17 (CaMKII)
 4,029 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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 alpha-methyl-glucopyranoside (alpha-MG) uptake nor Na+ uptake. The DEX-induced inhibition of Pi uptake was due to a decrease of V(max). In contrast, other steroid hormones such as progesterone, testosterone, and 17beta-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.
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PMID:Regulatory mechanism of polarized membrane transport by glucocorticoid in renal proximal tubule cells: involvement of [Ca2+]i. 1059 76