Excessive aldosterone secretion in some hypertensive patients may resu
lt 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 t
ransient transfections with murine AS/human growth hormone reporter co
nstructs. An angiotensin response element increasing AS gene transcrip
tion during angiotensin stimulation appears to reside within the initi
al 425 nt of the murine AS promoter. We also noted the possible presen
ce of a negatively-acting cis element between nt -425 and -1500. These
studies provide an initial step toward characterizing molecular mecha
nisms by which angiotensin regulates AS gene transcription.