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Introduction: Hypertension (HTN) causes cardiovascular disease. Despite this, many patients do not achieve blood pressure (BP) control. We hypothesized that non-diabetic hypertensive subjects with difficult-to-control BP will activate predictive signaling pathways. Methods: We collected demographics and 24-h and first-morning urine collections from 61 subjects enrolled in the Systolic Blood Pressure Intervention Trial (SPRINT). A validated instrument was administered to asses sugar sweetened beverage intake and converted to grams fructose per day. The BP-Difficult (BPD) group had SBP >140 mmHg or >120 mmHg for intensive group subjects, or BP at “goal” for the trial group and more than the median number of agents in each group in study as a whole. The “BP Easy” group (BPE) comprised the remainder of subjects. Mean BP from two visits before SPRINT termination established the study BP. Gene expression from transcriptomic sequencing of cellular RNAs of first-morning urine were assessed for differential expression (DE) genes (>1.5-fold change; P <0.01) by the Wilcoxon Rank-Sum test and pathway analysis. 354erd Results: Recoverable RNA from 51 subjects was present in 33 BPD and 18 BPE subjects. In the BPD group, 338 genes were upregulated and 3 downregulated; pathway analysis identified interferon, phosphoinositide 3-kinase, B cell receptor, and inducible nitric oxide synthase signaling as key upregulated pathways ( P <0.05). Most upregulated genes were components of pro-inflammatory pathways: interferon (IFNAR1), interleukin-2 and -4 (IL2RG, IL4R), tumor necrosis factor receptor (TNFRSF1B), and infiltrating B lymphocytes (PIK3AP1). BPD subjects with low 24-h urine sodium (<200 mmol) and fructose intake (<40 g/day) had 59 DE genes: 57 upregulated and 2 downregulated. Significant pathways included STAT3 and Cdc42 signaling pathways ( P <0.05), and IL2RG, MAPK14, TGFB1, and IFNAR1 were components of these pathways. Conclusions: Urinary cells from a difficult-to-control BP SPRINT cohort demonstrated molecular signatures associated with specific pro-inflammatory pathways and immune mediators.

Objective. To assess effi ciency of in hypertensive men capable of working. Design. Clinical study and instrumental (Ageing Male Score, AMS) examination were performed in 15 hypertensive men aged 32,8 ± 6,9 years old. Results and conclusions. Target blood pressure was achieved in 14 hypertensive men treated with eprosartan 600 mg/hydrochlorthiazide 12,5 mg during six month. Moreover, this therapy was associated with a signifi cant increase of normotonic reaction rate at physical load during veloergometry, and a signifi cant reduction in symptoms of androgen defi cit assessed by AMS in men.