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Chronic vagal nerve stimulation prevents high-salt diet-induced endothelial dysfunction and aortic stiffening in stroke-prone spontaneously hypertensive rats
Journal article   Open access   Peer reviewed

Chronic vagal nerve stimulation prevents high-salt diet-induced endothelial dysfunction and aortic stiffening in stroke-prone spontaneously hypertensive rats

Mark W Chapleau, Diane L Rotella, John J Reho, Kamal Rahmouni and Harald M Stauss
American journal of physiology. Heart and circulatory physiology, Vol.311(1), pp.H276-H285
07/01/2016
DOI: 10.1152/ajpheart.00043.2016
PMCID: PMC4967207
PMID: 27208157
url
https://doi.org/10.1152/ajpheart.00043.2016View
Published (Version of record) Open Access

Abstract

Parasympathetic activity is often reduced in hypertension and can elicit anti-inflammatory mechanisms. Thus we hypothesized that chronic vagal nerve stimulation (VNS) may alleviate cardiovascular end-organ damage in stroke-prone spontaneously hypertensive rats. Vagal nerve stimulators were implanted, a high-salt diet initiated, and the stimulators turned on (VNS, n = 10) or left off (sham, n = 14) for 4 wk. Arterial pressure increased equally in both groups. After 4 wk, endothelial function, assessed by in vivo imaging of the long posterior ciliary artery (LPCA) after stimulation (pilocarpine) and inhibition (N(ω)-nitro-l-arginine methyl ester) of endothelial nitric oxide synthase (eNOS), had significantly declined (-2.3 ± 1.2 μm, P < 0.05) in sham, but was maintained (-0.7 ± 0.8 μm, nonsignificant) in VNS. Furthermore, aortic eNOS activation (phosphorylated to total eNOS protein content ratio) was greater in VNS (0.83 ± 0.07) than in sham (0.47 ± 0.08, P < 0.05). After only 3 wk, ultrasound imaging of the aorta demonstrated decreased aortic strain (-9.7 ± 2.2%, P < 0.05) and distensibility (-2.39 ± 0.49 1,000/mmHg, P < 0.05) and increased pulse-wave velocity (+2.4 ± 0.7 m/s, P < 0.05) in sham but not in VNS (-3.8 ± 3.8%, -0.70 ± 1.4 1,000/mmHg, and +0.1 ± 0.7 m/s, all nonsignificant). Interleukin (IL)-6 serum concentrations tended to be higher in VNS than in sham (34.3 ± 8.3 vs. 16.1 ± 4.6 pg/ml, P = 0.06), and positive correlations were found between NO-dependent relaxation of the LPCA and serum levels of IL-6 (r = +0.70, P < 0.05) and IL-10 (r = +0.56, P < 0.05) and between aortic eNOS activation and IL-10 (r = +0.48, P < 0.05). In conclusion, chronic VNS prevents hypertension-induced endothelial dysfunction and aortic stiffening in an animal model of severe hypertension. We speculate that anti-inflammatory mechanisms may contribute to these effects.
 Phosphorylation Ciliary Arteries - metabolism Male Vagus Nerve Stimulation - instrumentation Implantable Neurostimulators Stroke - physiopathology Vasodilation Hypertension - blood Arterial Pressure Time Factors Interleukin-6 - blood Hypertension - therapy Nitric Oxide Synthase Type III - metabolism Vascular Stiffness Disease Models, Animal Rats, Inbred SHR Severity of Illness Index Heart Rate Stroke - prevention & control Endothelium, Vascular - physiopathology Aorta, Thoracic - metabolism Ciliary Arteries - physiopathology Aorta, Thoracic - physiopathology Sodium Chloride, Dietary Hypertension - physiopathology Stroke - etiology Animals Endothelium, Vascular - metabolism Hypertension - complications Enzyme Activation Nitric Oxide - metabolism Vagus Nerve Stimulation - methods

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