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Effects of anti‐hypertensive interventions on the inflammatory response in the spontaneously hypertensive rat
Author(s) -
Marvar Paul J,
McBryde Fiona D,
Paton Julian F.R.
Publication year - 2013
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.27.1_supplement.905.8
Subject(s) - denervation , medicine , blood pressure , immune system , autonomic nervous system , inflammation , sympathetic nervous system , endocrinology , heart rate , immunology
Clinical and pre‐clinical studies have found inflammation to be a contributing factor in the genesis of various forms hypertension. Current clinical interventions, such as renal denervation, target the autonomic nervous system to treat hypertension, however the effects of these blood pressure lowering strategies on the immune system are unknown. The current study examined immune cell activation and tissue infiltration following autonomic denervation procedures in an animal model of neurogenic hypertension. As determined by flow cytometry, the spontaneously hypertensive rat (SHR) exhibited a significant increase in the percentage of T lymphocytes (CD3+) in both the brainstem (3.3 ± 0.4 vs 1.6 ± 0.2; p=0.003) and aortic tissue (17.2 ± 1.6 vs 9.9 ± 2.1; p=0.01) compared to the normotensive control. These animals then underwent either renal denervation (RD) or carotid sinus denervation (CSD). Blood pressure in the SHR was significantly lowered following both RD and CSD. Compared to non‐denervated SHR, the total circulating leukocytes (CD45+) and CD3+ cells were attenuated following blood pressure lowering in the RD and CSD groups (p<0.001). These data suggest that reducing blood pressure with procedures targeting the autonomic nervous system is paralleled by reductions in tissue inflammation associated with hypertension. Supported by NIH‐HL107675–01, Marie Curie‐IIF – 276147 and British Heart Foundation.