Increased responsiveness of the carotid bodies to acute hypoxia was shown in animals exposed to chronic intermittent hypoxia (CIH). The kidney is sensitive to hypoxia and decreased cortical partial pressure of oxygen (PO2 ) levels was revealed in rats exposed to moderate CIH. We hypothesized that the response of the renal sympathetic nerve activity (RSNA) to acute hypoxia and hypercapnia is enhanced in rats exposed to CIH. Wistar rats were exposed to 96 cycles of CIH (6% O2 , 8 hr/day, n=6) or to normoxia (sham, 21% O2 , n=9) for 14 days. On day 15, rats were anesthetized (induction: urethane, α-chloralose and sodium pentobarbitone mixture i.p. (416, 27 and 33mg/kg), maintenance: urethane and α-chloralose mixture i.v. (62 and 4mg/kg)) to record cardiovascular parameters and RSNA. Rats were provided with supplementary oxygen to maintain PO2 levels > 84 mmHg. During hypoxia, rats breathed 10% O2 for two minutes. This was followed with a hypercapnic challenge during which rats breathed 10% CO2 for 5 minutes. Following a 90-minute recovery period, capsaizepine (CPZ, 5µg/ml/hr), a TRPV1 blocker, was infused into the right kidney. Then, hypoxic and hypercapnic challenges were repeated following the intra-renal infusion of CPZ. Data are expressed as mean±SD and were analyzed using t-test or ANOVA, where relevant. CIH rats were hypertensive (130±9 vs. 118±9mmHg, p=0.039) with comparable basal HR (425±38 vs. 407±34bpm), and RSNA (% of max, 33±12 vs. 25±12) compared with sham rats. In response to acute hypoxia, RSNA was increased to an equivalent extent in CIH-exposed and sham rats (Maximum change in RSNA of baseline, 128±23 vs. 125±16%; RSNA (% of max), 36±7 vs. 44±22%). Additionally, the increase in HR in response to acute hypoxia was similar between CIH-exposed and sham rats (∆HR, +42±29 vs. +30±27bpm). Mean arterial blood pressure (MAP) was similarly decreased in CIH-exposed and sham rats during acute hypoxia (Maximum change in MAP, -33±24 vs. -27±17mmHg). The decrease in PaO2 levels during hypoxia was comparable between exposure groups (∆PaO2 , -48±15 vs. -47±10mmHg). Hypercapnia induced a comparable increase in the RSNA in CIH-exposed and sham rats (Maximum change in RSNA of baseline, +121±15 vs. +113±8%). The analysis of absolute RSNA when normalized to maximum RSNA showed that CIH-exposed rats had increased RSNA compared with sham rats before and after exposure to hypercapnia (RSNA (% of max), 37±8 vs. 26±10%, p=0.037). The increase in PaCO2 levels during hypercapnia was similar between CIH and sham groups (∆PaCO2 , +24±8 vs. +19±6mmHg). Intra-renal CPZ did not alter the increase in RSNA and HR in response to hypoxia and hypercapnia in CIH-exposed and sham rats. Protein expression of TRPV1 receptors in kidney tissue was equivalent in both exposure groups (1.88±0.23 vs. 1.68±0.26ng/mg). Our results indicate that the responsiveness of RSNA to acute hypoxia and hypercapnia is not altered following exposure to moderate CIH sufficient to increase RSNA and blood pressure.