Abstract

Cardiovascular disease (CVD) is the leading cause of death in the United States. One of the primary risk factors for CVD is a lack of regular exercise. The brain controls the activity of the autonomic nervous system, which regulates many physiological functions; including blood pressure. The rostral ventrolateral medulla (RVLM) is an important region in the brainstem for blood pressure control because it contains a critical subset of adrenergic (C1) neurons that project to sympathetic preganglionic neurons in the spinal cord. C1 neurons from sedentary rats show more dendritic branching than in active rats, suggesting a novel mechanism by which inactivity could increase sympathetic activity and contribute to hypertension. However, it is also possible that the absolute number of C1 neurons changes along with the number of dendritic branches in sedentary rats. Therefore, the purpose of this study was to test the hypothesis that there are more C1 neurons in the RVLM of rats living under sedentary conditions compared to freely exercising rats. Aiming to understand the mechanisms by which inactivity leads to hypertension, we maintained four‐week old, male Sprague‐Dawley rats for 10–12 weeks under either physically active conditions (running wheels; 410±5.6 km total per rat) or sedentary conditions (no running wheels). Following perfusion and post‐fixation, sections of brainstem were first immunoperoxidase‐stained black for phenylethanolamine N‐methyltransferase (PNMT), a synthetic enzyme and marker of C1 neurons, and then brown for tyrosine hydroxylase (TH), the enzyme that all catecholamine neurons contain. PNMT+TH and TH only neurons in each rat were counted in the 6 sections containing the 600 μm caudal to the caudal pole of the facial nucleus (FN). Sedentary conditions did not produce a difference in the number, or rostrocaudal pattern, of C1 neurons compared to the active group nor an interaction between the two (two way RM ANOVA, p>0.05 ea). Sedentary conditions also did not affect the low number of TH neurons (likely A1 neurons) in the RVLM compared to active rats (2±1 vs. 2±1, respectively). Because the number of RVLM C1 neurons is the same in active and sedentary rats, we can exclude the possibility that an increase in the number of C1 neurons is a cause of increased activation of vasomotor spinal neurons and that structural neuroplasticity in C1 neurons may underlie increased functional excitability of the RVLM in our other studies. Future functional neuroanatomical studies using Fos protein should show whether the overall activation of the population of C1 neurons differs between sedentary and active rats.Support or Funding Information(HL096787‐09)This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

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