The effect of sodium deprivation and of angiotensin II infusion on the peripheral plasma concentrations of 18-hydroxycorticosterone, aldosterone and other corticosteroids in man

18-Hydroxy-11-Deoxycorticosterone Response to ACTH, Insulin and Furosemide Administration in Essential Hypertensive Patients

“…Following hydrosaline depletion with furosemide no significant varia tions in plasma 18-OH-DOC levels were observed in either normal subjects or EH patients, in agreement with the findings of Dale et al [ 15] and Mason et al [17], Other investigators [6,7,16], on the contrary, found a significant increase in plasma 18-OH-DOC during prolonged sodium restriction. This discrepancy may be explained by the fact that in the present study plasma samples were collected after administration of furosemide per os over a 12-hour period and not after 5 days of low sodium diet.…”

Control of Aldosterone Secretion

“…Infusion into normal subjects, whether sodium replete or deplete, raises the plasma concentrations of aldosterone and 18-hydroxycorticosterone but not those of other corticosteroids (Mason, Fraser, Morton, Semple & Wilson, 1976;Mason, Fraser, Morton, Semple & Wilson, 1977). In isolated zona glomerulosa cells, increases in aldosterone production are accompanied by parallel rises in the production of its precursors (Tait et al, 1974b;Bing & Schulster, 1977).…”

Plasma Levels of Aldosterone Precursors (Including the 18-Hydroxylated Compounds in this Synthesis Pathway) – A Tool for the Analysis of Adrenal Disorders?

“…Like aldoste rone, it is increased by upright posture and suppressed by high sodium intake, since the activity of the renin-angio tensin system is also depressed. The effect of angiotensin 11 is not secondary to increased ACTH secretion, since it is not affected by dexamethasone [18], Effect on 18-OHDOC. In agreement with other ste roids of zona fasciculata-reticularis origin, angiotensin II and changes in sodium status have no effect on 18-OHDOC secretion [20].…”

“…High sodium intake reduces 18-OHB production, and sodium restriction results in an increase in 18-OHB which parallels that of aldosterone, whereas DOC and B are unaffected [18]. The administra tion of diuretics stimulates 18-OHB production [24|.…”