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: Studies on capacitative calcium entry in vascular smooth muscle cells by measuring 45CA2+ influx. Author: Skutella M, Rüegg UT. Journal: J Recept Signal Transduct Res; 1997; 17(1-3):163-75. PubMed ID: 9029488. Abstract: Capacitative calcium entry was studied in the A7r5 vascular smooth muscle cell line by measuring 45Ca2+ influx. Entry was induced by depletion of the Ca2+ pools by either the receptor agonist [Arg]8 vasopressin (AVP) or the SR-Ca(2+)-ATPase inhibitor thapsigargin (TG). TG showed a higher efficacy for calcium influx than AVP. This is probably due to a larger Ca2+ release from the pools induced by TG compared to AVP and the irreversible inhibition of the SR-Ca(2+)-ATPase by TG causing influx to persist for a longer period of time. At maximally effective concentrations signals induced by AVP and TG were synergistic in the absence but not in the presence of the intracellular calcium chelator, 1,2-bis(2-aminophenoxy) ethane-N,N,N',N'-tetraacetic acid (BAPTA). Depolarisation with 55 mM KCl completely inhibited 45Ca2+ influx induced by TG but only slightly the one induced by AVP, both effects being less pronounced in the presence of BAPTA. [Ca2+]c signals induced by AVP and TG were both inhibited by depolarisation. In conclusion, although our results show differences between AVP- and TG- induced Ca2+ influx, they can be explained by their different mechanism of action and are in accordance with an activation of the same capacitative entry pathway by both agents.[Abstract] [Full Text] [Related] [New Search]