The baroreflex is a prominent moment-to-moment mechanism regulating the blood pressure. The hippocampus is a limbic structure in which has been pointed out as part of central network regulating baroreflex. However, the local neurochemical mechanisms involved in control of baroreflex function are not completely understood. Thus, this study aimed to investigate the involvement of nitrergic neurotransmission present in the dorsal hippocampus in baroreflex control of heart rate in conscious rats. For this, we evaluated the effect of bilateral microinjection into the dorsal hippocampus of either the
nitric oxide (NO) scavenger
carboxy-PTIO, the selective
neuronal nitric oxide synthase (nNOS) inhibitor Nω-Propyl-
l-arginine (NPLA) or the selective
inducible nitric oxide synthase (iNOS) inhibitor 1400 W in
bradycardia evoked by blood pressure increases in response to
intravenous infusion of
phenylephrine, and
tachycardia caused by blood pressure decreases evoked by
intravenous infusion of
sodium nitroprusside. Bilateral microinjection of
carboxy-PTIO into the dorsal hippocampus decreased the baroreflex tachycardic response without affecting the reflex
bradycardia. Hippocampus treatment with NPLA increased the baroreflex
bradycardia gain without affecting the reflex
tachycardia. Bilateral hippocampal treatment with 1400 W decreased the reflex
tachycardia and increased the baroreflex bradycardic response. Overall, these findings provide evidence that hippocampal nitrergic mechanisms acting in a NOS
isoform-specific manner plays a prominent role in control of baroreflex function. Indeed, the results indicate that nNOS and iNOS exerts an inhibitory influence on reflex
bradycardia, whereas iNOS mediates the reflex
tachycardia.