Exercise training in rats with heart failure significantly restored nNOS-positive neurons in the PVN (129 vs 99) and augmented renal sympathetic nerve activity responses (33% vs 20%).
Does exercise training improve endogenous nitric oxide mechanisms within the paraventricular nucleus in rats with heart failure?
Exercise training improves the altered nitric oxide mechanism within the paraventricular nucleus and restores NO-mediated changes in renal sympathetic nerve activity in rats with heart failure.
Tasa de eventos absoluta: 33% vs 20%
Previously, we have demonstrated that an altered endogenous nitric oxide (NO) mechanism within the paraventricular nucleus (PVN) contributes to increased renal sympathetic nerve activity (RSNA) in heart failure (HF) rats. The goal of this study was to examine the effect of exercise training (ExT) in improving the endogenous NO mechanism within the PVN involved in the regulation of RSNA in rats with HF. ExT significantly restored the decreased number of neuronal NO synthase (nNOS)-positive neurons in the PVN (129 +/- 17 vs. 99 +/- 6). nNOS mRNA expression and protein levels in the PVN were also significantly increased in HF-ExT rats compared with HF-sedentary rats. To examine the functional role of NO within the PVN, an inhibitor of NOS, N(G)-monomethyl-L-arginine, was microinjected into the PVN. Dose-dependent increases in RSNA, arterial blood pressure (BP), and heart rate (HR) were produced in all rats. There was a blunted increase in these parameters in HF rats compared with the sham-operated rats. ExT significantly augmented RSNA responses in rats with HF (33% vs. 20% at the highest dose), thus normalizing the responses. The NO donor sodium nitroprusside, microinjected into the PVN, produced dose-dependent decreases in RSNA, BP, and HR in both sham and HF rats. ExT significantly improved the blunted decrease in RSNA in HF rats (36% vs. 17% at the highest dose). In conclusion, our data indicate that ExT improves the altered NO mechanism within the PVN and restores NO-mediated changes in RSNA in rats with HF.
Zheng et al. (Fri,) conducted a other in Heart failure. Exercise training vs. Sedentary was evaluated on Renal sympathetic nerve activity (RSNA) response to NOS inhibitor at highest dose. Exercise training in rats with heart failure significantly restored nNOS-positive neurons in the PVN (129 vs 99) and augmented renal sympathetic nerve activity responses (33% vs 20%).