Abstract 201: Direct but not Indirect Activation of Sympathetic Ganglia Leads to Higher Neuronal Activation in Normotensive Than Deoxycorticosterone-salt Hypertensive Rats

Abstract

Sympathetic activity is chronically elevated in hypertensive human patients and in many animal models of hypertension, including the deoxycorticosterone (DOCA)-salt rat model. Sympathetic ganglia receive signals from the central nervous system and relay them to blood vessels and peripheral organs. How sympathetic ganglia respond to activation signals differently in hypertension is not fully understood. We examined how direct and indirect activators of sympathetic ganglia would influence neuronal activation. 2-deoxy-D-glucose (2-DG) is a glucose analog that causes hypoglycemia leading to centrally-mediated, indirect activation of celiac ganglia, a prevertebral sympathetic ganglion. Nicotine directly activates sympathetic ganglia by acting on cholinergic receptors found on most sympathetic neurons. Acute neuronal activation was examined by measuring c-fos immunoreactivity (ir). We hypothesized that since there is higher chronic sympathetic activity in DOCA-salt hypertensive than normotensive rats, both direct and indirect acute activators will induce higher c-fos expression in sympathetic ganglia of normotensive than hypertensive rats. Maximal c-fos expression for 2-DG (800mg/kg i.p.) and nicotine (2mg/kg s.c.) treatments was observed 2hrs post-treatment and for all following experiments, celiac ganglia were dissected and fixed 2hrs post-treatment. Following nicotine treatment, c-fos expression was significantly higher in celiac ganglia of normotensive (25.5 ± 9.7 c-fos ir neurons/m^2) than hypertensive (12.0 ± 4.8 c-fos ir neurons/m^2) rats. However, following 2-DG treatment, c-fos expression was similar in celiac ganglia of normotensive (49.1 ± 17.6 c-fos ir neurons/m^2) and hypertensive (49.4 ± 16.0 c-fos ir neurons/m^2). In contrast with our hypothesis, only the direct but not the indirect activation of sympathetic ganglia induced higher sympathetic neuronal activation in normotensive than hypertensive rats. Thus, a centrally-mediated metabolic stimulus does not activate pathways to sympathetic ganglia differentially in normotension versus hypertension. However, direct ganglionic stimulation leads to greater neuronal activation in normotensive than hypertensive ganglia.