Why the study?
Does dopamine blockade affect the ANP and natriuretic response to extracellular volume expansion in normal humans?
Does dopamine blockade affect the ANP and natriuretic response to extracellular volume expansion in normal humans?
Intrarenal dopamine and raised plasma ANP contribute to the natriuretic response to extracellular volume expansion, though they do not fully explain the underlying mechanisms.
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May support dopamine's independent role in natriuresis; hypothesis-generating and should not change practice.
The role of atrial natriuretic peptide (ANP) in the extracellular volume expansion (ECVE) induced natriuresis was examined in normal man under basal conditions and following dopamine blockage. Hypotonic ECVE was induced by drinking of 20 ml/kg tap water and subsequent intravenous infusion of 2 1 0, 9% saline over a period of 4 hours. This maneuver caused an increase in the plasma concentrations of ANP from 25.8 +/- 3.4 (means +/- SEM) to 59.7 +/- 6.7 fmol/ml. There was a dissociation between ANP response and urinary sodium excretion. A transient rise in glomerular filtration rate (GFR), plasma dopamine and a continuous decrease in plasma renin activity, aldosterone, vasopressin, and noradrenaline were observed. The natriuretic response to ECVE was blunted during dopamine blockade by metoclopramide, but plasma ANP, renin activity, catecholamine and vasopressin levels were not affected. However, plasma aldosterone rose. Our data are compatible with the concept that intrarenal dopamine and raised plasma concentration of ANP contribute to the natriuretic response to ECVE, but these hormonal changes do not completely explain the underlying mechanisms.
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Tulassay et al. (1988) studied this question.
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