Good J, Frost G, Oakley C M, Cleland J G
Department of Medicine (Cardiology), Royal Postgraduate Medical School, Hammersmith Hospital, London, UK.
Postgrad Med J. 1992;68 Suppl 2:S7-11.
Although an extensive literature exists on factors controlling sodium excretion in animal experimental models of heart failure, the relevance of these to the human condition remains largely unexplored. Increased renal sympathetic stimulation is considered responsible for heightened urinary sodium retention. Stimulation of dopamine receptors is believed to cause a diuresis. Accordingly, we sought to explore the influence of dobutamine (a beta-1 receptor agonist) and dopamine in high and low doses on a frusemide-induced diuresis in patients with chronic stable heart failure. Preliminary results indicate that low doses of dobutamine and dopamine do not increase a moderate, frusemide-induced diuresis. With higher doses dobutamine, but not dopamine, increased urine volume and sodium excretion. These results suggest that direct stimulation of beta-1 receptors increases urinary sodium excretion, either by a direct effect on the kidney or by altering systemic and renal haemodynamics.
