Abstract
Arterial baroreflex is a general mechanism maintaining cardiovascular homeostasis; its sensitivity is reduced in vascular calcification (VC). Hydrogen sulfide (H2S) treatment facilitates baroreflexive sensitivity in normal and hypertensive rats. Here, we aimed to detect the effect of H2S on baroreflexive sensitivity in rats with VC. The rat VC model was induced by vitamin D3 plus nicotine for 4 weeks. The sensitivity of baroreflex was detected by perfusing the isolated carotid sinus. VC was assessed by hematoxylin and eosin (H&E) staining, Ca2+ content and alkaline phosphatase (ALP) activity. Protein levels were detected by western blot analysis. Vitamin D3 plus nicotine induced structural disorder and elevated Ca2+ content in the aortic and carotid arterial wall and increased plasma ALP activity. In the calcified aorta and carotid artery, protein levels of contractile phenotype markers of vascular smooth muscle cells (VSMCs) were downregulated and that of osteoblast-like phenotype markers and endoplasmic reticulum stress (ERS) markers were upregulated. NaHS treatment ameliorated the histologic disorder and Ca2+ content in the calcified aorta and carotid artery, inhibited the elevated plasma ALP activity, and prevented the transformation of the VSMC phenotype and activation of ERS in rats with VC. Chronic NaHS treatment prevented the impairment of the baroreflex sensitivity and acute NaHS treatment dose-dependently improved the sensitivity in rats with VC. Our results suggested that H2S could directly facilitate the impairment of baroreflex in rats with VC and ameliorate VC, which might provide new target and strategy for regulation of the baroreflex and therapy of VC.
Highlights
Ectopic calcification, calcium crystal deposition in soft tissues, is a universal vascular pathophenotype linked with aging, hypertension, atherosclerotic cardiovascular diseases, diabetes, and chronic kidney disease (Leopold, 2015)
Baroreflex sensitivity is considered a comprehensive marker of the universal integrity of the autonomic nervous system (Robinson and Carr, 2002), which can be regulated by many endogenous active substances, such as angiotensin II and H2S (Zhang et al, 2015)
Reduced baroreflex sensitivity has been reported in patients with Vascular calcification (VC) and chronic kidney disease (Chesterton et al, 2005), which may contribute to dysfunction of the cardiovascular system and increased mortality (McIntyre, 2007; Kaur et al, 2016)
Summary
Calcium crystal deposition in soft tissues, is a universal vascular pathophenotype linked with aging, hypertension, atherosclerotic cardiovascular diseases, diabetes, and chronic kidney disease (Leopold, 2015). In the homeostatic mechanism arterial baroreflex, vascular, and cardiac function are modulated via detection of a change in tension in arterial vascular walls. The baroreflex arc consists basically of an afferent element, central neural element, and autonomic neuroeffector element. The baroreceptors are the major afferent elements of the reflex arc, which are sensors in the arterial walls mainly consisting of the aortic and carotid baroreceptor. The sensors detect the mechanical modification of arterial walls by afferent nervous terminals and trigger the excitation of these afferent nerves. Baroreflex sensitivity is considered a comprehensive marker of the universal integrity of the autonomic nervous system (Robinson and Carr, 2002), which can be regulated by many endogenous active substances, such as angiotensin II and H2S (Zhang et al, 2015)
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