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Increased oxidative stress underlies attenuated flow-induced dilation in cerebral resistance arteries of Sprague-Dawley rats on a high salt diet

High salt (NaCl) dietary intake is well known risk factor for the development of hypertension and microvascular dysfunction, leading to organ damage and increasing the risk of cardiovascular events. Endothelial function is impaired with HS dietary intake prior to increases in blood pressure. Novel studies suggest that this impairment is related to suppressed levels of angiotensin II, which has permissive, modulatory effect on the mechanisms of endothelial function via various vasodilatory and vasocontrictory pathways. Recently we demonstrated that short-term HS diet (4%NaCl in regular rat chow for 7 days) leads to attenuated flow-induced dilation (FID) of middle cerebral arteries (MCA) of normotensive Sprague Dawley rats, related to increased vascular oxidative stress (decreased cerebral vessels antioxidant enzymes’ expression) (J Physiol 2016 ; 594(17):4917-31). Increased superoxide/reactive oxygen species levels affect the vascular NO levels which are decreased in HS fed rats, assessed by direct fluorescence. HS intake changes FID mechanisms to, albeit reduced, entirely NO dependent, in contrast to the low-salt diet-fed group, where FID is NO, prostanoid, and epoxyeicosatrienoic acid dependent. Plasma lipid peroxidation products are increased in HS diet-fed rats, together with increased expression of transcription factor HIF-1α and VEGF. In vivo ROS scavenging by TEMPOL restores FID in HS diet-fed rats and ameliorates HS-induced increases in the HIF-1α and its downstream target genes (AJP 2018 ; 315(3):H718-H730). Finally, HS diet causes increased oxidative stress in leukocytes of peripheral lymph organs suggesting the ongoing low-grade inflammatory processes (J Physiol. 2016 ; 594(17):4917-31). Support: Croatian Science Fundation grant #IP-2014-09-6380.

NaCl, oxidative stress, microcirculation, Sprague-Dawley rats

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