Unresponsiveness of plasma mineralocorticoids to angiotensin II in diabetic patients with asymptomatic normoreninemic hypoaldosteronism
Kigoshi, T.; Morimoto, S.; Uchida, K.; Hosojima, H.; Yamamoto, I.; Imaizumi, N.; Azukizawa, S.
Journal of Laboratory and Clinical Medicine 105(2): 195-200
1985
ISSN/ISBN: 0022-2143 PMID: 2982980 Document Number: 261430
Isolated hypoaldosteronism with or without hyperkalemia in patients with diabetes mellitus was shown to exist occasionally without hyporeninemia. To assess in detail the adrenal function in this disorder, the responses of plasma aldosterone (PA) and its precursor steroids to angiotensin II (AII) infusion and ACTH injection were studied in 7 patients with asymptomatic normoreninemic hypoaldosteronism (ANH) and 11 age-matched normal subjects. The ANH diabetic patients had, by definition, a low PA level after furosemide (80 mg orally) plus upright posture (4 h) stimulation, low PA and high plasma renin activity (PRA) increases after the stimulation (a low .DELTA.PA/.DELTA.PRA ratio) and normokalemia. Plasma inactive renin and the inactive renin/total renin ratio were similar in the ANH diabetic patients and in the normal subjects. Under the pre-All condition, plasma DOC [11-deoxycorticosterone] and corticosterone levels tended to be low, and the plasma 18-OHB [18-hydroxycorticosterone] and PA levels were low in the ANH diabetic patients compared with the normal subjects. The ratio of plasma 18-0HB to PA was similar in the 2 groups. All infusion produced no increases in plasma 18-OHB and PA in the ANH diabetic patients; the infusion caused dose-dependent increases in these steroids in the normal subjects. Plasma DOC and corticosterone levels remained unchanged during all infusion in the 2 groups. ACTH injection produced appropriate PA increases relative to the basal PA in the 2 groups. Apparently, diabetic patients with ANH have selective unresponsiveness of the zona glomerulosa, probably involving the All receptors and the aldosterone biosynthetic enzymes, to All but not to ACTH.