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Cui Hong

First Clinical Institute，China Medical University. Shenyang 110001,Liaoning, China

Abstract

In HEK293 cell lines in which α1a-, α1b- or α1d-adrenoceptor subtypes were stably expressed, fluorescence intensities due to traces of Ca2+ were investigated using fura-2/ AM with the aim of exploring signal transduction pathways of intracellular Ca2+ increase mediated by these receptor subtypes. Pertussis toxin had no effect on [ Ca2+ j, increase mediated by all three subdues of α1-adrenoceptors. However, U-73122 and PMA could inhibited the [ Ca2+ ], increase induced by NE, which was not affected by Foskolin and RP-cAMPs. Pretreatment with calphostin C abolished the [ Ca2+ ], response tO PMA.Quercetin and twhostin inhabited maximal [ Ca2+ ], increase but had no effect on the plateau phase in all the three transfected cells. In the HEK293 cells, the phosphatideCa2+ signalling system mediated by the 3 subtypes of al-AR was brought into play by activation of phospholiphase C via coupling with PIX-insensitive G proteins.

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Citing This Article：

Cui Hong. . Acta Physiol Sin 1998; 50 (3): (in Chinese with English abstract).