In normotensive Sprague-Dawley rats and Wistar-Kyoto (WKY) rats stimulation of renal mechanoreceptors or chemoreceptors by increasing ureteral pressure or renal pelvic perfusion with 0.9 M NaCl results in a contralateral inhibitory renorenal reflex response with contralateral diuresis and natriuresis. However, in 14–15-week-old spontaneously hypertensive rats (SHR) renal sensory receptor stimulation failed to elicit a contralateral inhibitory renorenal reflex response. The present study was performed to examine whether the lack of a renorenal reflex response in SHR was related to elevated arterial pressure by studying the responses to renal sensory receptor stimulation in 5–6-week-old SHR and in 12–16-week-old SHR that had been treated with captopril from 3 weeks of age to prevent the development of hypertension. In 5–6-week-old SHR, mean arterial pressure was 113±3 mm Hg. Graded increases of ureteral pressure of 15 and 29 mm Hg resulted in graded increases in ipsilateral afferent renal nerve activity of 57±22% and 120±38%. Contralateral urinary sodium excretion increased from 0.26±0.06 to 0.35±0.07 μmol/min/g and from 0.36±0.08 to 0.46±0.11 μmol/min/g, respectively. In captopril-treated SHR, mean arterial pressure was 109±3 mm Hg. Increasing ureteral pressure by 34 mm Hg increased ipsilateral afferent renal nerve activity 65±21% and contralateral urinary sodium excretion from 1.28±0.24 to 1.53±0.30 μmol/min/g. Similar results were produced by renal chemoreceptor stimulation. It is concluded that renal sensory receptor stimulation results in a contralateral inhibitory renorenal reflex response in 5–6-week-old SHR and in SHR treated with captopril to prevent the development of hypertension. These results suggest that the previously demonstrated lack of a renorenal reflex response to renal sensory receptor stimulation hi hypertensive SHR is related to the maintenance of hypertension.