In anesthetized rats, stimulating renal mechanoreceptors (MR) by increasing renal venous pressure (RVP) 22 mmHg increased ipsilateral (ipsi) renal vascular resistance (RVR) from 23.5 to 31.3 mmHg/(ml X min-1 X g-1), ipsi urinary sodium excretion (UNaV) from 0.26 to 0.49 mumol X min-1 X g-1, contralateral (contra) urine flow rate (V) from 3.13 to 4.43 microliter X min-1 X g-1, and UNaV from 0.30 to 0.46 mumol X min-1 X g-1. Ipsi renal denervation (DNX) did not affect the increase in ipsi RVR but reduced the increase in ipsi UNaV. The increases in contra V and UNaV were abolished by either ipsi or contra renal DNX. Increases RVP increased ipsi afferent renal nerve activity (ARNA) 288 counts/10 s and decreased ipsi and contra efferent renal nerve activity (ERNA) 242 and 490 counts/10 s, respectively. Renal pelvic instillation of lidocaine (5 micrograms/ml) did not affect the renal functional or electrophysiological responses to increases RVP but abolished the increase in ipsi ARNA, the decrease in contra ERNA, and the increases in contra V and UNaV produced by increasing ureteral pressure (UP) or retrograde ureteropelvic perfusion with 0.9 M NaCl [chemoreceptor (CR) stimulation]. Chronic T6 spinal cord section abolished the increase in ipsi ARNA, the decrease in contra ERNA, and the increases in contra V and UNaV produced by renal MR (increases RVP, increases UP) and CR stimulation. We conclude increases that RVP results in an ipsi and contra inhibitory renorenal reflex. Differential blockade with pelvic lidocaine suggests that the sensory receptors activated by increases RVP are located in an anatomically different area than those activated by increases UP or retrograde ureteropelvic perfusion with 0.9 M NaCl. An intact spinal cord is required for the normal responsiveness of renal sensory neuroreceptor complexes to specific stimuli in the context of the complete renorenal reflex response.