Cardiopulmonary baroreceptor input is necessary for brain Fos expression following ETB receptor activation

Abstract

In vivo stimulation of ETB receptors produces a pattern of neuronal activation similar to that observed in isotonic volume expansion (VE). Both protocols significantly increased Fos expression, a nuclear marker of neural activity, in brain regions important for the maintenance of cardiovascular homeostasis (nucleus of the solitary tract, NTS; caudal ventrolateral medulla, CVLM; paraventricular nucleus, PVN; supraoptic nucleus, SON). Cunningham et al (2002) reported that this central nervous system response to VE primarily involved input from cardiac afferents in the heart. The goal our present study is to establish the contribution of cardiac receptors to the pattern of neuronal activation caused by ETB receptor activation. To achieve this goal, we reduced/abolished input from cardiopulmonary receptors in male Sprague-Dawley rats by bilateral kainic acid (KA) deafferentation of the nodose ganglia. Both sham and chemically denervated KA animals then received iv infusions of either isotonic saline at 0.01 ml/min or the ETB receptor agonist sarafotoxin 6c (S6c) at a rate of 5pmol/kg/min for 2 h. At the end of the infusion period, brains were processed for Fos immunocytochemistry. Mean arterial pressures of S6c infused rats increased significantly compared to saline in both sham and KA rats. KA deafferentation significantly decreased Fos expression produced by S6c infusion in the PVN and NTS with lesser reductions in the SON, CVLM. In conclusion, part of the neural response to ETB receptor activation is dependent on cardiopulmonary afferents input. Our research is supported by NIH P01HL-70687.