Exaggerated pressor and sympathetic nerve responses during spontaneously‐occurring motor activity in decerebrate spontaneously hypertensive rats

Abstract

Stimulation of the mesencephalic locomotor region (a putative component of the central command pathway) has been shown to elicit exaggerated pressor and sympathetic nerve responses in decerebrate spontaneously hypertensive rats (SHR) as compared to normotensive Wister-Kyoto rats. This finding suggests that central command activity and/or influence on caudal vasomotor centers may be augmented in hypertension. In the normotensive decerebrate rat model, mean arterial pressure (MAP) and sympathetic nerve activity are known to increase during intermittent bouts of spontaneous motor activity. Moreover, evidence suggests that simulated central command influences at the brainstem may evoke these pressor and sympathetic responses. However, it remains unknown whether these spontaneous changes in cardiovascular hemodynamics are altered with the pathogenesis of hypertension. Based on this background, we hypothesized that the pressor and sympathetic nerve responses during spontaneously-occurring motor activity are exaggerated in hypertension. MAP, renal sympathetic nerve activity (RSNA), and tibial nerve discharge were measured in decerebrate SHR (n=8) and normotensive Sprague-Dawley (SD) rats (n=6). The present study aimed to compare resting baroreflex changes in RSNA (in response to pharmacological alterations in MAP) and central command-evoked responses in MAP and RSNA during spontaneously-occurring motor activity between SHR and normotensive SD. Results demonstrated that the baroreflex-mediated RSNA response was not different between SHR and SD. In both SHR and SD, abrupt, spontaneous increases in RSNA were synchronized with tibial motor discharge and followed by a rise in MAP. These potentially central command-evoked increases in MAP and RSNA were greater in SHR than SD. Phenylephrine-induced elevations in MAP did not suppress the central command-induced RSNA increase in SHR, whereas it abolished the rise in RSNA in SD. Taken together, it is concluded that 1) the arterial baroreflex is operative during resting conditions in SHR as well as SD; 2) the pressor and sympathetic nerve responses during spontaneously-occurring motor activity are exaggerated in hypertensive rats; and 3) exaggerated RSNA responses in SHR may be induced along a central command pathway independent of the arterial baroreflex and/or as a result of central command-induced inhibition of the arterial baroreflex itself.