Differential roles of hippocampal nNOS and iNOS in the control of baroreflex function in conscious rats

Abstract

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.