Discharge of RVLM vasomotor neurons is not increased in anesthetized angiotensin II-salt hypertensive rats

作者：Pedrino Gustavo R; Calderon Alfredo S; Andrade Mary Ann; Cravo Sergio L; Toney Glenn M^*

来源：American Journal of Physiology - Heart and Circulatory Physiology, 2013, 305(12): H1781-H1789.

DOI：10.1152/ajpheart.00657.2013

• angiotensin II
• high-salt diet
• hypertension
• rostral ventrolateral medulla vasomotor neurons
• single unit recording
• sympathetic nerve activity

Neurons of the rostral ventrolateral medulla (RVLM) are critical for generating and regulating sympathetic nerve activity (SNA). Systemic administration of ANG II combined with a high-salt diet induces hypertension that is postulated to involve elevated SNA. However, a functional role for RVLM vasomotor neurons in ANG II-salt hypertension has not been established. Here we tested the hypothesis that RVLM vasomotor neurons have exaggerated resting discharge in rats with ANG II-salt hypertension. Rats in the hypertensive (HT) group consumed a high-salt (2% NaCl) diet and received an infusion of ANG II (150 ng.kg(-1).min(-1) sc) for 14 days. Rats in the normotensive (NT) group consumed a normal salt (0.4% NaCl) diet and were infused with normal saline. Telemetric recordings in conscious rats revealed that mean arterial pressure (MAP) was significantly increased in HT compared with NT rats (P < 0.001). Under anesthesia (urethane/chloralose), MAP remained elevated in HT compared with NT rats (P < 0.01). Extracellular single unit recordings in HT (n = 28) and NT (n = 22) rats revealed that barosensitive RVLM neurons in both groups (HT, 23 cells; NT, 34 cells) had similar cardiac rhythmicity and resting discharge. However, a greater (P < 0.01) increase of MAP was needed to silence discharge of neurons in HT (17 cells, 44 +/- 5 mmHg) than in NT (28 cells, 29 +/- 3 mmHg) rats. Maximum firing rates during arterial baroreceptor unloading were similar across groups. We conclude that heightened resting discharge of sympathoexcitatory RVLM neurons is not required for maintenance of neurogenic ANG II-salt hypertension.

• 出版日期2013-12