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Selective Beneficial Effects of Chronic Vagal Nerve Stimulation (VNS) on Vascular Function in Stroke‐Prone Spontaneously Hypertensive Rats (SHR‐SP) on High‐Salt Diet
Abstract   Open access   Peer reviewed

Selective Beneficial Effects of Chronic Vagal Nerve Stimulation (VNS) on Vascular Function in Stroke‐Prone Spontaneously Hypertensive Rats (SHR‐SP) on High‐Salt Diet

Erin E Meyers, Mark W Chapleau, Kamal Rahmouni and Harald Martin Stauss
The FASEB journal, Vol.30(S1)
04/2016
DOI: 10.1096/fasebj.30.1_supplement.1237.7
url
https://doi.org/10.1096/fasebj.30.1_supplement.1237.7View
Published (Version of record) Open Access

Abstract

Abstract only Increased sympathetic nervous system activity contributes to the pathogenesis of essential hypertension and has been identified as an independent risk factor for cardiac and vascular end‐organ damage in hypertension. On the other hand, heart rate variability is often reduced in hypertension, suggesting decreased parasympathetic modulation of cardiac function. Since parasympathetic nervous system activity has been linked to anti‐inflammatory actions, we tested the hypothesis that restoring parasympathetic nervous system activity by chronic VNS attenuates development of cardiac and vascular end‐organ damage in SHR‐SP on high‐salt diet. Telemetric blood pressure sensors and vagal nerve stimulators were chronically implanted in SHR‐SP (10 weeks of age, n=20). A high‐salt diet (1% NaCl in drinking water) was initiated in all animals, and the vagal nerve stimulators were turned on (VNS group, n=9) or left off (sham stimulation group, n=11) for 4 weeks. VNS delayed weight gain without affecting food or water intake, suggesting increased metabolic rate. Heart rate did not change over the 4‐week observation period and did not differ between groups. Systolic blood pressure increased from 173±4 mmHg and 174±5 mmHg to 204±12 mmHg (VNS) and 204±10 mmHg (Sham) respectively, with no difference between groups. Endothelial‐mediated arterial dilation was assessed by in vivo imaging of the long posterior ciliary artery (LPCA). The difference of the lumen diameter of the LPCA after corneal application of pilocarpine (causes release of nitric oxide (NO) from endothelial cells via activation of muscarinic receptors) and after corneal application of L‐NAME (endothelial NO synthase inhibitor) was used as an index of endothelial‐mediated arterial dilation. After 4 weeks of high‐salt diet endothelial‐mediated arterial dilation had significantly declined (−2.9±1.4 μm, P<0.05) in sham stimulated SHR‐SP but was maintained (−0.8±0.9 μm, NS) in SHR‐SP with VNS. After only 3 weeks of high‐salt diet, aortic pulse wave velocity assessed by echocardiographic determination of aortic strain and measurement of pulse pressure had significantly increased from 6.1±0.7 m/s to 8.3±0.7 m/s (P<0.05) in sham stimulated SHR‐SP but was maintained (5.2±0.9 m/s vs. 5.6±0.4 m/s, NS) in SHR‐SP with VNS, suggesting less aortic stiffening in rats with VNS. Left ventricular mass assessed by echocardiography and vascular hypertrophy assessed by wall to lumen ratio of the LPCA both increased significantly over the 4‐week observation period but did not differ between groups. In conclusion, chronic VNS prevents high‐salt diet‐induced endothelial dysfunction and aortic stiffening in an animal model of severe hypertension without affecting blood pressure or cardiac and vascular hypertrophy. We speculate that the anti‐inflammatory effect of chronic VNS may potentially contribute to this beneficial vascular effect of chronic VNS in SHR‐SP on high‐salt diet. Support or Funding Information Supported by a pilot grant from the University of Iowa Hospitals and Clinics Center for Hypertension Research.

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