NO in the caudal NTS modulates the increase in respiratory frequency in response to chemoreflex activation in awake rats.

The role of nitric oxide (NO) in the caudal NTS (cNTS) on baseline cardiovascular and respiratory parameters and on changes in respiratory frequency (fR) and cardiovascular responses to chemoreflex activation was evaluated in awake rats. Bilateral microinjections of l-NAME (200nmoles/50nL), a non-selective NO synthase (NOS) inhibitor, into the cNTS increased baseline arterial pressure, while microinjections of N-PLA (3pmoles/50nL), a selective neuronal NOS (nNOS) inhibitor, did not. l-NAME or N-PLA microinjected into the cNTS reduced the increase in fR in response to chemoreflex activation but not cardiovascular responses. These data show that (a) NO produced by non-nNOS in the cNTS is involved in the baseline autonomic control and (b) NO produced by nNOS in the cNTS is involved in modulation of the increase in fR in response to chemoreflex activation but not in the cardiovascular responses. We conclude that NO produced by the neuronal and endothelial NOS play a different role in the cNTS neurons integral to autonomic and respiratory pathways.