Sodium molybdate prevents hypertension and vascular prostanoid imbalance in fructose‐overloaded rats

Abstract

(1) Fructose (F) overload produces elevated blood pressure (BP), hyperglycaemia, hypertriglyceridemia and insulin resistance, resembling human metabolic syndrome. Previously, we found altered vascular prostanoid (PR) production in this model. (2) Sodium molybdate (Mo), as well as sodium tungstate, causes insulin-like effects and normalizes plasma glucose levels in streptozotocin-treated diabetic rats. We studied the effects of Mo on BP, metabolic parameters and release of PR from the mesenteric vascular bed (MVB) in F-overloaded rats. (3) Four groups of male Sprague-Dawley rats were analysed: Control, tap water to drink; F, F solution 10% W/V to drink; CMo, Mo 100 mg kg day(-1) and FMo, both treatments. After 9 weeks, the animals were killed and MVBs removed and the released PRs measured. (4) F increased BP, glycemia, triglyceridemia and insulinemia. Mo treatment prevented the increases in BP and glycemia, but did not modify triglyceridemia or insulinemia. In addition, Mo decreased BP in controls. (5) Prostaglandins (PG) F2 alpha and E2, PG 6-ketoF1 alpha and thromboxane (TX) B2 , as well as inactive metabolites of prostacyclin (PGI2 ) and TXA2 were detected. F decreased the production of vasodilator PRs PGI2 and PGE2 in MVB. Mo prevented these alterations and increased PGE2 in controls. Vasoconstrict or PRs PGF2 alpha and TXA2 release was not modified. (6) Mo treatment, beyond its known lowering effect on glycemia, prevents the reduction in the vascular release of vasodilator PR observed in this model. This could be one of the mechanisms by which Mo avoids the increase in BP caused by F overload in the rat.

Inhibition of the JAK2/STAT3/SOSC1 Signaling Pathway Improves Secretion Function of Vascular Endothelial Cells in a Rat Model of Pregnancy-Induced Hypertension

“…NO, PGI2, ET, TXA2 are vasoactive substances secreted by vascular endothelial cells and are involved in the regulation of vascular tone and proliferation of vascular smooth muscle cells [37]. Notably, these factors are important factors in the development of hypertension and prostanoid imbalance [38]. Xu et al found that the NO and 6-keto-PGF1a levels were decreased and endothelia and TXB2 levels were increased in spontaneously hypertensive rats, which is consistent with our results [39].…”

Metal biomarker mixtures and blood pressure in the United States: cross-sectional findings from the 1999-2006 National Health and Nutrition Examination Survey (NHANES)

“…Our current results support findings from a previous analysis of NHANES survey cycle data from 1999 to 2012, which found that Cs was associated with lower SBP and DBP [38], and results from a small epidemiological study of particulate matter (PM) constituents, which found negative associations between Mo and SBP/DBP [39]. Two studies in rat models also support that exposure to Cs [40] and Mo [41] may reduce BP. However, results from other studies have yielded different conclusions: two NHANES analyses (2009-2012 and 2011-2012 cycles) identified positive associations of Cs and Mo with high BP [36,42], and a study of aging men with metabolic syndrome found no significant Spearman correlation between urinary Mo and SBP or DBP [43].…”

Inverse Association of Plasma Molybdenum with Metabolic Syndrome in a Chinese Adult Population: A Case-Control Study

“…Plasma molybdenum and other essential elements concentrations were detected by inductively coupled plasma mass spectrometry (Agilent 7700 Series ICP-MS; Tokyo, Japan) in the Ministry of Education Key Laboratory of Environment and Health at Tongji Medical College of Huazhong University of Science and Technology, as described in our previous study [32]. In the daily measurement, specimens from MetS cases and control subjects were randomly assayed.…”