Involvement of nitric oxide (NO) in the nucleus tractus solitarii (NTS) on respiratory but not in cardiovascular responses to chemoreflex activation in awake rats

Abstract

There is evidence that NO is a neuromodulator in the NTS. In the present study we evaluated the effect of nitric oxide synthase (NOS) inhibition in the caudal nucleus tractus solitarii (cNTS) on: a) the baseline cardiovascular and respiratory functions, and b) the changes on mean arterial pressure (MAP), heart rate (HR) and respiratory frequency (RF) in response to chemoreflex activation in awake rats. Rats received bilateral guide‐cannulas in the cNTS and the femoral artery and vein were cannulated. RF was evaluated by body‐plethysmography. Chemoreflex was activated with KCN (iv) before and after bilateral microinjections of a non‐selective NOS inhibitor L‐NAME (n=8) or a selective neuronal NOS inhibitor N‐Propyl (n=7) into cNTS. Microinjection of L‐NAME into cNTS produced a significant increase in baseline MAP (100 ± 2 vs 112 ± 3 mmHg) but no changes in HR and RF. Microinjection of N‐Propyl into cNTS did not affect baseline MAP, HR and RF. Microinjection of L‐NAME (138 ± 10 vs 81 ± 11 cpm) or N‐Propyl (159 ± 13 vs 90 ± 17 cpm) into cNTS significantly reduced the tachypneic but had no effect on the magnitude of cardiovascular responses to chemoreflex. The data shows that the activation of the respiratory component of the chemorreflex in the caudal NTS involves nNOS‐derived NO production, while NO does not modulate the cardiovascular responses. Supported by CNPq and FAPESP.