Abstract:
:Cultured pulmonary artery endothelial (CPAE) cells possess specific high affinity receptors for atrial natriuretic peptide (ANP). CPAE cells were used to investigate the regulation of ANP receptors by glucocorticoids. Treatment of CPAE cells with dexamethasone (1 microM) produced a 69.3 +/- 23% (P less than 0.01) increase in the maximum binding of [125I]ANP to CPAE cells without affecting the affinity of binding. The EC50 for the dexamethasone effect was approximately or equal to 0.5 nM, with a maximum effect at 10 nM. The effect was time dependent and developed over 16-72 h, and it could be inhibited by cycloheximide (0.075 micrograms/ml), indicating a requirement for de novo protein synthesis. The glucocorticoid receptor antagonist RU 486 completely inhibited the dexamethasone effect. In affinity cross-linking experiments, dexamethasone increased the labelling of the ANP-R2, or clearance, receptor, whereas labeling of the ANP-R1 receptor could not be detected. Despite the increase in maximum binding, dexamethasone treatment produced a significant (P less than 0.01) decrease in the ANP-stimulated cyclic GMP response of CPAE cells and no change in the affinity of binding for the truncated ANP analog, atriopeptin I. These results indicate that the dexamethasone effect is mediated through glucocorticoid receptors and may be selective for the nonguanylate cyclase-coupled, or ANP-R2, receptor subtype. This study provides direct evidence for regulation of ANP receptors by steroid hormones.
journal_name
Endocrinologyjournal_title
Endocrinologyauthors
Lanier-Smith KL,Currie MGdoi
10.1210/endo-129-5-2311subject
Has Abstractpub_date
1991-11-01 00:00:00pages
2311-7issue
5eissn
0013-7227issn
1945-7170journal_volume
129pub_type
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