Abstract
Salusin-β is a bioactive peptide involved in vascular smooth muscle cell proliferation, vascular fibrosis and hypertension. The present study was designed to determine the effects of silencing salusin-β on hypertension and cardiovascular remodeling in spontaneously hypertensive rats (SHR). Thirteen-week-old male SHR and normotensive Wistar-Kyoto rats (WKY) were subjected to intravenous injection of PBS, adenoviral vectors encoding salusin-β shRNA (Ad-Sal-shRNA) or a scramble shRNA. Salusin-β levels in plasma, myocardium and mesenteric artery were increased in SHR. Silencing salusin-β had no significant effect on blood pressure in WKY, but reduced blood pressure in SHR. It reduced the ratio of left ventricle weight to body weight, cross-sectional areas of cardiocytes and perivascular fibrosis, and decreased the media thickness and the media/lumen ratio of arteries in SHR. Silencing salusin-β almost normalized plasma norepinephrine and angiotensin II levels in SHR. It prevented the upregulation of angiotensin II and AT1 receptors, and reduced the NAD(P)H oxidase activity and superoxide anion levels in myocardium and mesenteric artery of SHR. Knockdown of salusin-β attenuated cell proliferation and fibrosis in vascular smooth muscle cells from SHR. These results indicate that silencing salusin-β attenuates hypertension and cardiovascular remodeling in SHR.
Highlights
vascular smooth muscle cells (VSMCs) migration and intimal hyperplasia after vascular injury[17]
The salusin-β contents in the hypothalamic paraventricular nucleus (PVN) and rostral ventrolateral medulla (RVLM) of the brain was increased in Spontaneously hypertensive rats (SHR), intravenous administration of Ad-SalshRNA had no significant effect on the salusin-β contents in the PVN and RVLM (Fig. 1C)
The measurements were carried out 2 weeks after intravenous injection of PBS, adenoviral vectors encoding scramble shRNA (Ad-Scr-shRNA) or salusin-β shRNA (Ad-Sal-shRNA). (A) Representative transverse section images with Masson’s stain. (B) Bar graph showing the media thickness, lumen diameter and the ratio of media thickness to lumen diameter
Summary
VSMCs migration and intimal hyperplasia after vascular injury[17]. It stimulates human VSMCs proliferation via cAMP-PKA-EGFR-CREB/ERK pathway, and causes vascular fibrosis via TGF-β1-Smad pathway[10]. It is unknown whether endogenous salusin-β plays a role in the pathogenesis of hypertension and cardiovascular remodeling. Hypertensive rats (SHR) is a commonly used animal model of primary hypertension. SHR was used as a hypertension animal model in the present study. The aim of this study is to determine whether endogenous salusin-β contributes to hypertension and cardiovascular remodeling
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