Lack of inhibition of ACTH-induced aldosterone stimulation by Desasp-, ileu-angiotensin II in man.

Ikeda, Fumitake; Kono, Tsuyoshi; Oseko, Fumimaro; Imura, Hiroo; Endo, Jiro

doi:10.1507/endocrj1954.26.631

Cited by 1 publication

(3 citation statements)

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“…The aldosterone response to ACTH during both normal and low sodium intakes is not influenced by endogenous angiotensin II (5, 6). Elias et al (5) demonstrated that combined ACTH and saralasin (an angiotensin II analog) administration did not alter an ACTH‐induced rise in plasma aldosterone during sodium restriction in normal subjects.…”

Section: Discussionmentioning

confidence: 99%

“…Elias et al (5) demonstrated that combined ACTH and saralasin (an angiotensin II analog) administration did not alter an ACTH‐induced rise in plasma aldosterone during sodium restriction in normal subjects. Ikeda et al (6) found that simultaneous infusion of ACTH and desasp 1 ‐, ileu 8 ‐angiotensin II (an angiotensin III analog) did not inhibit a plasma aldosterone response to ACTH during a period of normal sodium intake in man. Therefore, the reduced aldosterone responsiveness to ACTH in sodium‐restricted elderly subjects may be entirely dependent upon the decrease in the basal secretory activity.…”

Section: Discussionmentioning

confidence: 99%

“…In a previous study, we demonstrated that elderly subjects also had a lesser plasma aldosterone response to exogenous angiotensin II, in parallel with decreases in basal plasma renin and aldosterone levels under conditions of low sodium intake in normotensive subjects (4). However, it recently has been suggested that the plasma aldosterone response to exogenous ACTH during both normal and low sodium intakes is not influenced by endogenous angiotensin II in normal subjects (5, 6).…”

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Reduced Aldosterone Secretory Response to Acute ACTH Stimulation in Sodium‐Restricted Elderly Subjects

Morimoto

Takeda

Uchida

et al. 1980

J American Geriatrics Society

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The plasma aldosterone (PA) response to ACTH stimulation (5 μg/kg, im) under conditions of varied sodium intake was studied in 10 young (20–35 yr), 9 middle‐aged (41–56 yr) and 11 elderly (66–73 yr) normotensive subjects. No differences in serum sodium, serum potassium, plasma Cortisol and urinary sodium excretion were observed among the three groups during both a 130 mEq (normal) intake and a 25 mEq (low) sodium intake for three days. Basal plasma renin activity (PRA) and PA levels were lower in the elderly than in the young or middle‐aged groups. These age‐related decreases were slight with a normal sodium intake and pronounced with a low sodium intake. ACTH administration induced increases in PA in the three groups. However, the maximal net increment of PA above the baseline level after ACTH did not differ among the three groups with a normal sodium intake, but was lower in the elderly than in the young or middle‐aged groups with a low sodium intake. The ACTH‐induced maximal percentage increment of PA did not differ among the three groups during both the normal and the low sodium intakes. A significant positive correlation was found between the maximal net increment of PA and either the basal PRA or PA level in the combined group of young, middle‐aged and elderly subjects. Thus, aging causes a reduced aldosterone secretory response to ACTH, in parallel with decreases in basal PRA and PA levels, under conditions of low sodium intake.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

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