1980 Volume 56 Issue 7 Pages 973-982
To evaluate the dopaminergic control of aldosterone secretion, the following experiments were performed on 10 normal subjects (3 men and.7 women, aged 21-69 yrs.), 16 diabetics (8 men and 8 women, aged 20-74 yrs.) and 7 patients with untreated hyperthyroidism (2 men and 5 women aged 16-58 yrs.). Blood samples were withdrawn from an intravenous cannula indwelled in an antecubital vein at 0, 15, 30, 45, 60, 90 and 120 min after intravenous injection of 10mg metoclopramide with a volus. Plasma aldosterone levels and plasma renin activities (PRA) were measured by radioimmunoassay.
In normal subjects, plasma aldosterone levels were significantly increased from basal levels of 111.8±13.0pg/ml (Mean±S.E.) to 183.4±23.3pg/ml 15 min after an intravenous injection of metoclopramide and were sustained for about 90 min. This increase induced by metoclopramide was, however, abolished by pretreatment with 2.5mg of bromocriptine. It is suggested that metoclopramide and bromocriptine are in a competitive relationship at the level of dopaminergic receptor.
In diabetics, the mean plasma level of aldosterone was as low as 66.3±8.7pg/ml, which was significantly lower than that in normal subjects (p<0.01), and aldosterone response to metoclopramide was significantly diminished. Although this tendency was more apparent in diabetics with such complications as neuropathy or retinopathy, aldosterone response to metoclopramide implied that aldosterone secretion was under dopaminergic inhibition in this hypoaldosteronemic state.
While aldosterone responded well to metoclopramide, PRA was not significantly altered in this treatment in normal subjects and diabetics.
In patients with untreated hyperthyroidism, aldosterone response was similar to that in normal subjects.
