Journal of Hypertension

Skip Navigation LinksHome > March 2014 - Volume 32 - Issue 3 > Actions of rilmenidine on neurogenic hypertension in BPH/2J...
Journal of Hypertension:
doi: 10.1097/HJH.0000000000000036
ORIGINAL PAPERS: Neurogenic mechanisms

Actions of rilmenidine on neurogenic hypertension in BPH/2J genetically hypertensive mice

Jackson, Kristy L.a,b; Palma-Rigo, Kesiaa; Nguyen-Huu, Thu-Phuca; Davern, Pamela J.a,*; Head, Geoffrey A.a,b,*

Supplemental Author Material
Collapse Box


Objective: BPH/2J hypertensive mice have an exaggerated sympathetic contribution to blood pressure (BP). Premotor sympathetic neurons within the rostroventrolateral medulla (RVLM) are a major source of sympathetic vasomotor tone and major site of action of the centrally acting sympatholytic agent, rilmenidine. The relative cardiovascular effect of rilmenidine in BPH/2J versus normotensive BPN/3J mice was used as an indicator of the involvement of the RVLM in the sympathetic contribution to hypertension in BPH/2J mice.

Methods: BPH/2J and BPN/3J mice were pre-implanted with telemetry devices to measure BP in conscious unrestrained mice. Rilmenidine was administered acutely (n = 7–9/group), orally for 14 days, at a wide range of doses (n = 5/group), and also infused intracerebroventricularly for 7 days (n = 6/group).

Results: Acute intraperitoneal rilmenidine induced greater depressor and bradycardic responses in BPH/2J than BPN/3J mice (Pstrain < 0.01). Both responses were reduced by atropine pre-treatment, with the remaining hypotensive effect being small and comparable between strains (Pstrain = 1.0). This suggests that vagally induced reductions in cardiac output were responsible for the hypotension. Chronic intracerebroventricularly infused rilmenidine reduced BP from baseline marginally in BPH/2J mice during the dark (active) period (−6.5 ± 2 mmHg; P= 0.006). Chronic orally administered rilmenidine (1–12 mg/kg per day) also had minimal effect on 24-h BP in both strains (P > 0.16).

Conclusion: The sympathetic vasomotor inhibitory effect of rilmenidine is minimal in both strains and similar in hypertensive BPH/2J and BPN/3J mice. Thus, hypertension in BPH/2J mice is not likely mediated by greater neuronal activity in the RVLM, and agents such as rilmenidine would be an ineffective treatment for this form of neurogenic hypertension.

© 2014 Wolters Kluwer Health | Lippincott Williams & Wilkins


Article Tools


Article Level Metrics

Search for Similar Articles
You may search for similar articles that contain these same keywords or you may modify the keyword list to augment your search.