In:
Acta Endocrinologica, Oxford University Press (OUP), Vol. 125, No. 6 ( 1991-12), p. 694-699
Abstract:
Since thyroid hormones have been reported to increase the synthesis of rat atrial natriuretic hormone and its mRNA accumulation, we further investigated the mechanism of stimulation of rANH synthesis by T 3 using cultured rat atrial myocytes. T 3 (10 −9 -10 −7 mol/l) increased cellular content and secretion into the medium of immunoreactive rANH in a dose-dependent manner. However, the ratio of secreted/cellular rANH was not altered by the addition of T 3 . Furthermore, in both cellular and secreted rANH, the larger molecular form (γ-rANH) apparently predominated over the smaller one (α-rANH), and this profile was not influenced by T 3 (10 −7 mol/l). Although T 3 (10 −9 -10 −7 mol/l) also increased cellular rANH mRNA accumulation, the ratio of cellular rANH/rANH mRNA was not changed. Moreover, using actinomycin D, we found that T 3 (10 −7 mol/l) did not affect the degradation of rANH mRNA. From these findings, we suggest that T 3 has no specific effects on the translational and posttranslational processes and the release of rANH, but that T 3 stimulates rANH synthesis in the pretranslational levels, probably in the transcriptional level of rANH gene.
Type of Medium:
Online Resource
ISSN:
0804-4643
,
1479-683X
DOI:
10.1530/acta.0.1250694
Language:
Unknown
Publisher:
Oxford University Press (OUP)
Publication Date:
1991
detail.hit.zdb_id:
1485160-X
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