Baroreflex Modulation by Physical Training: Involvement of nNOS in the Paraventricular Nucleus of Hypothalamus (PVN)

We evaluated the baroreflex and involvement of nNOS in the PVN in sedentary (Gsed) or trained animals (Gtr). Wistar male rats of Gsed or Gtr underwent guide cannulas implantation to PVN and catheterization of the femoral artery and vein to record mean arterial pressure (MAP) and heart rate (HR). Phenylephrine and sodium nitroprusside were infused before and after bilateral microinjection of nNOS inhibitor in the PVN. The nNOS expression in the PVN was analyzed by Real Time qPCR and the content of the isoforms PVNmedial (PVNm) and posterior (PVNp) by immunohistochemistry. At rest, the Gtr had bradycardia and increased baroreflex gain. The Gtr showed higher variation of MAP (Gsed: 53 ± 2 vs. Gtr: 66 ± 4 mmHg) and HR (Gsed: ‐84 ± 1 vs. Gtr: ‐94 ± 0,9bpm) with phenylephrine. After nNOS inhibition, the differences were abolished (ΔPAM: Gsed: 55 ± 1 vs. Gtr: 54 ± 1 mmHg) and (ΔFC: Gsed: ‐99 ± 6 vs. Gtr: ‐99 ± 6 bpm). Variations in MAP and HR with sodium nitroprusside were higher in Gtr before (ΔPAM: Gsed: ‐22 ± 2 vs. Gtr: ‐44 ± 1 mmHg / ΔFC: Gsed: 108 ± 3 vs. Gtr: 142 ± 3 bpm) and after (ΔPAM: Gsed: ‐24 ± 3 Gtr: ‐42 ± 3 mmHg / ΔFC: Gsed: Gtr 100 ± 3: 150 ± 3 bpm) nNOS inhibition. The training induced higher nNOS gene expression and increased the amount of immunoreactive cells in PVNm. Our data indicate that swimming training modulates baroreflex gain due in part to nNOS increase in the PVN.