Modulation of natriuresis and renal dopamine excretion by sympathetic activity and the renin-angiotensin-aldosterone system.

The involvement of the sympathetic nervous system and the renin-angiotensin-aldosterone system in renal dopamine (DA) synthesis and sodium excretion (UNaV) were studied in 11 healthy volunteers. On a low sodium diet (LoSo, 50 mmol Na+) saline infusions were given without pretreatment or after oral intake of 50 mg captopril or 300 micrograms clonidine. On a high sodium diet (HiSo, 250 mmol Na+) saline was infused without or after intake of 300 micrograms clonidine. UNaV, the excretion rates of the DA precursor 3,4-dihydroxyphenylalanine (DOPA; UDOPAV), DA (UDAV), and noradrenaline (NA; UNAV), hormonal parameters, blood pressure (BP), glomerular filtration parameters, blood pressure (BP), glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured. Saline infusion alone during LoSo increased natriuresis without changes in catechol excretion or suppression of plasma renin activity (PRA) or plasma aldosterone (PALD). Sympatho-inhibition by clonidine resulted in marked antinatriuresis, decrease in BP and decrease in UDOPAV and UDAV, whereas plasma DOPA, GFR, and ERPF remained unchanged. PRA and PALD rose as indication of activation of the RAA system, probably by the reduced renal perfusion pressure after clonidine. Captopril significantly stimulated the saline-induced natriuresis without affecting UDOPAV and UDAV. On HiSo, when sympathetic tone is relatively suppressed, saline infusion alone stimulated natriuresis but did not affect catechol excretion or PRA. In the first and second hour after saline infusion PALD was suppressed. Clonidine again reduced BP and natriuresis, while PRA, PALD, and UDOPAV and UDAV were unaffected. These results suggest that sympathetic nerve activity may stimulate the intrarenal DA production.(ABSTRACT TRUNCATED AT 250 WORDS)