Aldosterone synthase gene regulation by angiotensin.
Excessive aldosterone secretion in some hypertensive patients may result from abnormal aldosterone synthase (AS) gene regulation in response to changes in dietary sodium intake. We have utilized NCI-H295 cells, which exhibit stable angiotensin-induced aldosterone secretion, for transient transfections with murine AS/human growth hormone reporter constructs. An angiotensin response element increasing AS gene transcription during angiotensin stimulation appears to reside within the initial 425 nt of the murine AS promoter. We also noted the possible presence of a negatively-acting cis element between nt -425 and -1500. These studies provide an initial step toward characterizing molecular mechanisms by which angiotensin regulates AS gene transcription.
Holland
O B
OB
Department of Internal Medicine, University of Texas Medical Branch, Galveston, USA.
Carr
B
B
Brasier
A R
AR
D000306:Adrenal Cortex Neoplasms / Q000235:genetics; D000804:Angiotensin II / Q000494:pharmacology*; D019405:Cytochrome P-450 CYP11B2; D003577:Cytochrome P-450 Enzyme System / Q000235:genetics*; D015971:Gene Expression Regulation, Enzymologic / Q000187:drug effects*; D005816:Genetic Complementation Test; D006801:Humans; D013252:Steroid 11-beta-Hydroxylase / Q000235:genetics*; D014407:Tumor Cells, Cultured
D000804:Angiotensin II; D003577:Cytochrome P-450 Enzyme System; D019405:Cytochrome P-450 CYP11B2; D013252:Steroid 11-beta-Hydroxylase