To determine the effects of long-term angiotensin-converting enzyme inhibition (ACEI) and blood pressure (BP) lowering on renal sodium transporter abundance and distribution in Spontaneously Hypertensive Rats (SHR), 9-wk SHR were treated with enalapril (30mg/kg.day) 4 wks. BP decreased from 156 ± 4 to 96 ± 8 mmHg. Na⁺/H⁺ exchanger isoform 3 (NHE3) and Na⁺-Pi cotransporter type 2 (NaPi2) localized to the body of the microvilli (MV) in normotensive rat strains. In untreated SHR NHE3 partially retracted from the body to base of the MV and NaPi2 retracted to sub apical vesicles. After enalapril treatment of SHR, NHE3 fully retracted to the base of the MV and, by density gradient fractionation, NHE3, NaPi2, dipeptidyl peptidase IV, myosin VI, Na-Cl cotransporter and cortical Na-K-Cl cotransporter redistributed from low density (apical enriched) to high density (endosome enriched) membranes. Enalapril decreased total abundance of myosin VI (to 0.51 ± 0.18 of untreated), ACE (0.67 ± 0.22), and cortical NaPi2 (0.83 ± 0.10). Normalizing SHR BP with HRH (hydralazine 7.5 mg/d, reserpine 0.15 mg/d and hydrochlorothiazide 3 mg/d) did not change Na⁺ transporter density distribution or abundance. We conclude that lowering BP to normal levels in SHR does not normalize Na⁺ transporter distribution, rather, chronic ACEI treatment provokes retraction of Na⁺ transporters and associated proteins from transport relevant domains of apical membranes and/or reduces their abundance.