Relationship between immunological alterations, hypoxia and inflammation in arterial hypertension combined with metabolic syndrome

Our study was aimed at assessing a relationship between immune system alterations, hypoxia and inflammation in arterial hypertension (AH) coupled to metabolic disturbances. A total of 117 patients were enrolled into clinical study, having been randomized into groups in accordance with study protocol, aged 30 to 62 years. They sought care in outpatient setting or underwent periodic health examination at the Republican Clinical Hospital №5, Saransk, Mordovia, Russia. A control group contained 25 apparently healthy subjects lacking signs of metabolic syndrome (MS) and elevated arterial pressure. A comparison group contained 47 patients with AH grade I-II featured with damaged target organs, but lacking associated relevant clinical manifestations, as based on the assay data. The main group contained 45 patients receiving antihypertensive therapy with overt AH grade I-II verified upon medical consultation coupled to damaged target organs and MS signs with its randomly combined components, but lacking associated clinical manifestations. The patients from main and comparison groups received antihypertensive therapy in accordance with approved guidelines and clinical recommendations for management of AH patients consisting of one of renin-angiotensin-aldosterone system blockers, diuretic and/or dihydropyridine calcium channel blocker. Cytokine profile, level of hypoxia and non-specific inflammation were measured in blood serum. The data obtained demonstrated that AH patients with/without metabolic syndrome were noted to display cytokine profile shifted towards elevated proand anti-inflammatory immune arm pointing at imbalanced immune regulation. Hypoxic changes were also found in blood serum that was confirmed by elevated level of lactic and pyruvic acid in these groups. Moreover, development of such pathology was coupled to hypoxia which served as a modulator of immune-related and non-specific inflammation. Rise of non-specific low-grade inflammation correlates developing irreversible AH-associated changes in organs, progression of atherosclerosis and accelerated cardio-metabolic continuum. Altogether, such alterations underlie pathogenetic mechanisms of tissue damage emerging upon AH and MS being mutually aggravating factor along with activated renin-angiotensin-aldosterone system.