Brainstem catecholaminergic neurons affect mean arterial pressure and heart rate at rest and during hypercapnic stress in conscious rats

Abstract

We hypothesize that brainstem catecholaminergic (CA) neurons contribute to sympathetic nervous system activity maintaining mean arterial pressure (MAP) and heart rate (HR) at rest and during stress. Here, we specifically lesion brainstem CA neurons in adult male Harlan Sprague-Dawley rats by injecting anti-dopamine-β-hydroxylase-saporin (DBH-SAP) into the fourth ventricle. Control rats are injected with IgG-saporin (IgG-SAP), producing no neural lesion. MAP, HR and sleep state are monitored both before and after the injection. This protocol decreases CA neurons at A5, A6, and A7 by 73–84% and at C1 and C2 by 56–60% (Li and Nattie, J. Physiol, in press). Two weeks following DBH-SAP injection compared to controls, lesioned rats have a 10% increase in MAP (P<0.01; two-way ANOVA) and a 13% increase in heart rate (P<0.01; two-way ANOVA). Exposure to 7% CO2 induces a 4% MAP decrease in lesioned rats compared to room air values while controls increase by 4%. The 8% MAP decrease in lesioned rats is significant compared to controls (P<0.01; two-way ANOVA). Finally, these trends do not differ between wake and NREM vigilance states. These results suggest that brainstem CA neurons seem to lower MAP and HR at rest. This outcome is unexpected if these neurons are involved in the sympathetic system. However, in accordance with out hypothesis, CA neurons appear to contribute to the elevation of MAP during hypercapnic stress. Support By: NIH HL 28066, Rosaline Borison Memorial Fund Predoctoral Fellowship, Albert J. Ryan Foundation Predoctoral Fellowship