Abstract
We studied whether therapeutic doses of cyclosporin A (CsA) modify the effects of nutrient and non-nutrient stimuli on pH i, in the insulin-secreting β-cell line HIT-T 15. Glucose caused a transient acidification, followed by alkanization. CsA failed to block this alkalinization. PMA elicited a gradual alkalinization by a protein kinase C mediated mechanism which is not inhibited by CsA. The despolarization with high K + was associated with a rise in PH i. CsA was able to completely block this increase in pH i. Ionomycin induced a rapid cytosolic alkalinization partially inhibited by CsA. We conclude that in HIT-T 15 cells therapeutical doses of CsA inhibit the Ca 2+-dependent pathway of Na +/H + antiport activation but not protein kinase C activation of this exchanger.
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
