Elevated renin substrate coupled with failure of suppression of circulating renin results in increased angiotensin I formation in patients with Cushing's syndrome, glucocorticoid therapy, or oral contraceptive use.
Supports differential renin substrate responses in glucocorticoid excess states; leaves open diagnostic utility and requires prospective validation.
Plasma renin activity and plasma renin substrate were measured by radioimmunoassay of generated angiotensin I in patients with steroid excess syndromes. Significant increases in substrate were observed in patients with Cushing's syndrome, during glucocorticoid therapy and on oral contraceptive agents. Suppression of plasma renin activity occurred only in primary aldosteronism. 2. The Michaelis constant (Km) for the reaction between renin and substrate in plasma at physiological pH (7.4) was also determined. The extent to which elevated plasma renin substrate increases the velocity of angiotensin I formation was then calculated. 3. In patients with Cushing's syndrome, glucocorticoid therapy or oral contraceptive use, elevated renin substrate coupled with failure of suppression of circulating renin results in increased angiotensin I formation.
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Krakoff et al. (1973) studied this question.
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