These tools will no longer be maintained as of December 31, 2024. Archived website can be found here. PubMed4Hh GitHub repository can be found here. Contact NLM Customer Service if you have questions.


Pubmed for Handhelds

PUBMED FOR HANDHELDS

Search MEDLINE/PubMed

  • Title: High glucose levels alter angiotensin II-induced Ca(2+) uptake via PKC and cAMP pathways in renal proximal tubular cells.
    Author: Park SH, Shin SS, Han HJ.
    Journal: Kidney Blood Press Res; 2001; 24(2):84-91. PubMed ID: 11435739.
    Abstract:
    Although a dysfunction of the calcium metabolism occurs in diabetes mellitus, alterations of Ca(2+) uptake induced by angiotensin II (ANG II) in renal proximal tubular cells (PTCs) grown in high-glucose medium are not fully elucidated. Thus, we examined whether high glucose concentrations can induce an alteration of the ANG II effect on the Ca(2+) uptake and its action mechanism in primary cultured renal PTCs. PTCs were exposed to different glucose concentrations (5-100 mM) and time intervals (0-48 h). There was a sustained increase of Ca(2+) uptake at glucose concentrations >15 mM. Thus, we selected 25 mM glucose and incubation for 48 h to maintain a hyperglycemic condition in vitro, unlike short-time regulatin. ANG II significantly inhibited the Ca(2+) uptake in a dose-dependent manner in a 5-mM glucose medium. In addition, downregulation of ANG II receptors appeared in a glucose dose dependent manner. However, PTCs treated with 25 mM glucose for 48 h, not 12 h, did not exhibit the inhibitory effect of ANG II (10(-7) M) on Ca(2+) uptake, although the inhibitory effect of ANG II on Ca(2+) uptake occurred in the presence of 25 mM mannitol or L-glucose. Staurosporine, bisindolylmaleimide I (protein kinase C, PKC, inhibitors), 12-o-tetradecanoylphorbol 13-acetate pretreatment, SQ 22536 (an adenylate cyclase inhibitor), and myristoylated protein kinase A inhibitor amide 14-22 (a protein kinase A inhibitor) blocked the 25-mM-glucose-induced alteration of ANG II effect on Ca(2+) uptake. These results suggest that both PKC and cyclic adenosine monophosphate (cAMP) pathways are involved in the high-glucose-induced alteration of ANG II effect on Ca(2+) uptake. Indeed, 25 mM glucose increased PKC activity and cAMP contents. In conclusion, a high glucose concentration altered ANG II induced inhibition of Ca(2+) uptake via PKC and cAMP pathways in the PTCs.
    [Abstract] [Full Text] [Related] [New Search]