A defective dopamine DA1 receptor has been suggested to be involved in the salt-sensitive hypertension in Dahl-S rats (DS). To investigate the consequences of this defect, the influence of DA1 receptor blockade (SCH23390) and of dopamine-synthesis inhibition (benserazide) on volume expansion (VE)-induced sodium and dopamine excretion was studied in anesthetized prehypertensive DS and salt-resistant Dahl rats (DR). Under control conditions all measured variables were equal in DR and DS. During VE (5% of BW), sodium and dopamine excretion increased similarly in the two strains. During peak natriuresis mean arterial blood pressure was 119 +/- 3 and 122 +/- 3 mm Hg, respectively. In DR treated with SCH23390, sodium excretion was only 72% of that in vehicle-treated DR. Dopamine excretion increased, however, as in vehicle-treated DR. In DS, treatment with SCH23390 did not attenuate natriuresis and dopamine excretion also increased as in vehicle-treated DS. In benserazide-pretreated DR and DS, sodium excretion during VE was similar, but only 50-51% of that in the respective vehicle-treated group. Dopamine excretion decreased by about 80% in both strains. In conclusion, prehypertensive DR and DS have a similar capacity to acutely excrete an intravenous saline load and to generate dopamine. The total dopamine involvement in VE-induced natriuresis is also comparable in the two strains, but the natriuresis mediated by DA1 receptors is pronounced in DR and non-existent in DS.(ABSTRACT TRUNCATED AT 250 WORDS)