Plasma
aldosterone,
18-hydroxycorticosterone (18-OH-B),
18-hydroxydeoxycorticosterone (18-OH-DOC),
corticosterone,
cortisol and
prolactin levels were determined during an
angiotensin II infusion at increasing rates both with and without a simultaneous infusion of
dopamine in seven normotensive subjects, in ten patients with
essential hypertension, and in ten patients with primary
aldosteronism. In a second set of experiments, maximum increases of these plasma levels were determined after
metoclopramide (10 mg intravenously) in all subgroups. As compared with the other groups, an exaggerated
angiotensin II-induced response of plasma
aldosterone and 18-OH-B levels was observed in the five patients with low-
renin essential hypertension (LREH) and in five patients with idiopathic
hyperaldosteronism (IHA).
Dopamine reduced the maximal increase of
aldosterone and of 18-OH-B after
angiotensin II to 259 +/- 48 (SEM) pg/ml and 511 +/- 152 pg/ml respectively in LREH (without
dopamine: 515 +/- 74 and 908 +/- 201 respectively; P less than 0.05), and to 466 +/- 197 and 741 +/- 212 in IHA (without
dopamine: 766 +/- 193 and 1264 +/- 337 respectively; P less than 0.05). The maximal increases of plasma
aldosterone, 18-OH-B, and
prolactin after
metoclopramide (10 mg intravenously) were higher (P less than 0.01) in patients with LREH and in patients with primary
aldosteronism. Plasma levels of 18-OH-DOC,
corticosterone and
cortisol were not affected by the stimuli applied. The exaggerated response to
metoclopramide as well as to
angiotensin II and its reversion only by pharmacological doses of
dopamine are consistent with an increased but ineffective
dopamine inhibition of
aldosterone and 18-OH-B in LREH and IHA.