Why the study?
Does dopaminergic blockade alter urinary sodium excretion and atrial natriuretic factor release during volume expansion in normal subjects?
Does dopaminergic blockade alter urinary sodium excretion and atrial natriuretic factor release during volume expansion in normal subjects?
Dopaminergic blockade blunts volume expansion-induced natriuresis independently of atrial natriuretic factor release, suggesting a role for type 2 dopaminergic receptors in this process.
May implicate D2 receptors in volume-induced natriuresis independent of ANF; hypothesis-generating for edematous states pending clinical studies.
Ten normal subjects were subjected to 2 h water immersion with and without pharmacological dopaminergic blockade with either metoclopramide (group I) or domperidone (group II). 2. In group I, urinary sodium excretion showed a marked increase during water immersion alone, whereas it was blunted during water immersion plus dopaminergic blockade with metoclopramide (P less than 0.05 vs water immersion alone, n = 5). Plasma aldosterone was significantly suppressed by water immersion alone (P less than 0.05), but remained unchanged during water immersion plus metoclopramide. Plasma atrial natriuretic factor showed similar augmentation during water immersion alone and during water immersion plus metoclopramide. 3. Another five subjects (group II) were studied during water immersion alone and during water immersion plus dopaminergic blockade with domperidone. In this group the increase in urinary sodium excretion was similarly blunted by dopaminergic blockade. Plasma atrial natriuretic factor was equally elevated during water immersion alone and during water immersion plus domperidone, but aldosterone was suppressed by both water immersion alone and water immersion plus domperidone. 4. Our findings suggest that water immersion-induced atrial natriuretic factor release is independent of dopaminergic activity. Dopamine blockade is able to blunt significantly both water immersion-induced natriuresis and plasma aldosterone suppression, independently of the marked elevation of circulating atrial natriuretic factor, via a mechanism involving type 2 dopaminergic receptors.
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Coruzzi et al. (1989) studied this question.
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