GLUTAMATE AND NITRIC OXIDE INTERACTION IN THE ROSTROVENTROLATERAL MEDULLA (RVLM) OF WISTAR RATS SUBMITTED TO EXERCISE TRAINING

We evaluate the participation of nitric oxide (NO) in the glutamatergic neurotransmission of rostroventrolateral medulla (RVLM) of awake rats sedentary or exercise trained. 33 Wistar rats weighting 220 to 250g were submitted to swimming training (Gtr) or sedentary (Gsed). After the last training session guide cannulae were implanted to the RVLM and after 3 days of recovery, cannulas to the femoral artery and vein were implanted for direct recording of mean arterial pressure (MAP) and heart rate (HR) 24 hours later with animals awake. Results showed bradycardia at rest for the Gtr compared to Gsed (GTr: 326.67±7.3 vs. Gsed: 349.63±4.9bpm) and a greater baroreflex gain (Gtr: −4.41±0.5 vs. Gsed: −2.42±0.31). The pressor response to glutamate in Gsed was increased compared to Gtr (Gsed: ÄMAP: 53±7.7mmHg vs. Gtr: ÄMAP: 32±4.2mmHg) and indifferent after microinjection of carboxy‐PTIO (Gsed: ÄMAP: 41±7.7mmHg vs. Gtr: ÄMAP: 39±5.9mmHg). The pressor response of glutamate in the Gsed before microinjection of n‐propyl was also increased compared to Gtr (Gsed: ÄMAP: 49±3.8mmHg vs. Gtr: ÄMAP: 36±3.9mmHg) and did not change after n‐propyl (Gsed: ÄMAP: 42±5mHg vs. Gtr: ÄMAP: 41±5.2mmHg). The data indicate that swimming can decrease sympathetic activity modifying glutamatergic neurotransmission in the RVLM. The removal of NO reversed those alterations, suggesting a role of NO in the RVLM during exercise training.