Dopamine is capable of modulating zona glomerulosa function. Of this there now seems little doubt. However, whether varying dopamine levels in vivo forms the basis of a realistic normal physiological control mechanism for aldosterone secretion is far from clear. Reviewers have been cautious (Ganguly, 1984) or enthusiastic (Sowers, 1984) depending on the choice of evidence and the weight given to individual studies, but some resolution of the uncertainty is pressing since aberrations in this as yet unproven relationship have been suggested as basic abnormalities in a number of forms of hypertensive disease.
Evidence for and against the dopamine–aldosterone relationship has been obtained using dopamine itself and antagonists or agonists of its action in whole animals and in tissue preparations. Initial impetus for the dopamine hypothesis came from the observation that the dopamine agonist, bromocriptine, inhibited the response of aldosterone to frusemide-induced sodium loss (Edwards, Thorner, Miall et al. 1975) although
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