Proenkephalin gene expression in the brainstem regulates post-exercise hypotension.

Abstract

The opioid receptor antagonist naloxone reverses the reduction in blood pressure following exercise. We have previously demonstrated that compared to genetically matched controls, spontaneously hypertensive rats (SHR) have decreased proenkephalin mRNA levels in the nucleus tractus solitarius (NTS), the caudal (CVLM) and rostral ventrolateral medulla (RVLM) of the brainstem. We hypothesized that in SHR an acute bout of exercise would increase proenkephalin mRNA in the NTS and RVLM. Female 12-week-old SHR (n = 4/group) were randomly assigned to exercise and control groups. Mean arterial pressure (MAP) and heart rate were recorded at rest and every 5 min for 30 min following: (1) 40 min of treadmill running at 30 m/min, 10% grade; or (2) 40 min of rest on the treadmill. Rats were sacrificed 30 min post-exercise or post-rest. Exercise induced increases in MAP and heart rate, approximately 18 mmHg and approximately 140 beats/min, respectively, P < 0.001. There were no differences in pre-exercise/rest MAP between groups, or in control rats following rest on the treadmill, 162.5 +/- 3 vs. 163.1 +/- 4 mmHg, control and control after treadmill rest, respectively; NS P > 0.05. The pre- to post-exercise reduction in MAP after 40 min of treadmill running was from 164 +/- 5.1 to 146 +/- 2.0 mmHg (P < 0.001) as recorded 30 min post-exercise. At 30 min post-exercise proenkephalin mRNA levels in the NTS, CVLM and RVLM were increased: 97, 198 and 227%, respectively, P < 0.01. These data reconfirm the existence of post-exercise hypotension in SHR and suggest that increases in enkephalin synthesis and release in the NTS, CVLM, and RVLM may be involved in regulating post-exercise hypotension.