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We compared the norepinephrine (NE) induced α1B-adrenoceptor (α1B-AR) expression modulation between two transfected human embryonic kidney (HEK) 293 cell lines in which α1B-AR densities were (6 336 ±913) and (773±164) fmol · mg -1, respectively. Treatment of cells with NE (10 μmol · L1) for 48 h decreased high-level expressed α1B-AR density, but increased low-level expressed α1B-AR density. The protein kinase C inhibitor Calphostin C or Ro-31-8220 reversed, and its activator PMA mimicked the NE-induced down-regulation of high-level expressed α1B-AR. Moreover, PMA induced a down-regulation of low-level expressed α1B-AR. The endoplasmic reticulum Ca2+-ATPase inhibitor cyclopiazonic acid (CPA) and the calcium chelator BAPTA/AM did not affect the down-regulation of high-level expressed α1B-AR, but inhibited the up-regulation of low-level expression α1B-AR induced by NE. These results suggest that α1B-adrenoceptor densities at different initial expression levels are differentially regulated by
We compared the norepinephrine (NE) induced α1B-adrenoceptor (α1B-AR) expression modulation between two transfected human embryonic kidney (HEK) 293 cell lines in which α1B-AR densities were (6 336 ± 913) and (773 ± 164) fmol · Mg -1, respectively. Treatment of cells with NE (10 μmol · L -1) for 48 h decreased high-level expressed α1B-AR density, but increased low-level expressed α1B-AR density. The protein kinase C inhibitor Calphostin C or Ro-31-8220 reversed, and its activator PMA mimicked the NE-induced down-regulation of high-level expressed α1B-AR. Moreover, PMA induced a down-regulation of low-level expressed α1B-AR. The endoplasmic reticulum Ca2 + ATPase inhibitor cyclopiazonic acid (CPA) and the calcium chelator BAPTA / AM did not affect the down-regulation of high-level expressed α1B-AR, but inhibited the up-regulation of low-level expression α1B-AR induced by NE. These results suggest that α1B-adrenoceptor densities at different initial expression levels are different ially regulated by