The effect of endothelin (ET)-1 infusion on renal hemodynamics and the tubuloglomerular feedback (TGF) mechanism was examined in rats. ET-1 reduced early proximal flow rate (EPFR) measured in the absence of distal flow from 28 +/- 1 to 23 +/- 1 nl/min at a subpressor dose (100 pmol.100 g body wt-1.h-1 iv) and from 27 +/- 2 to 19 +/- 2 nl/min at a pressor dose (200 pmol.100 g body wt-1.h-1). Reductions of EPFR induced by loop perfusion at 40 nl/min were 11 +/- 1 and 12 +/- 1 nl/min at the subpressor and pressor doses and were not different from controls. The stop-flow pressure response to loop perfusion was not altered by the pressor dose of ET-1. The subpressor dose of ET-1 increased renal vascular resistance (RVR) by 40% but left glomerular filtration rate (GFR) and urinary excretion of sodium (UNaV) unaltered. The pressor dose of ET-1 not only increased RVR by 140% and decreased GFR and renal plasma flow by 37 and 52%, but it increased UNaV proportional to the rise in blood pressure (r = 0.724, P less than 0.01). ET-1 is a potent renal vasoconstrictor and induces pressure natriuresis. ET-1 increases both pre- and postglomerular resistances but does not affect TGF response.