One of the novel interesting topics in the study of cardiovascular disease is the role of the oxidation system, since inflammation and oxidative stress are known to lead to cardiovascular diseases, their progression and complications. During decades of research, many complex interactions between agents of oxidative stress, oxidation, and antioxidant systems have been elucidated, and numerous important pathophysiological links to na number of disorders and diseases have been established. This review article will present the most relevant knowledge linking oxidative stress to vascular dysfunction and disease. The review will focus on the role of oxidative stress in endotheleial dysfunction, atherosclerosis, and other pathogenetic processes and mechanisms that contribute to the development of ischemic heart disease.

Hyperbaric oxygenation (HBO₂) can modify gene and protein expression, signaling pathways, and vascular function, leading to altered vasomotor responses. Adenosine receptors (ARs) may mediate these effects by modulating vasoactivity. This study investigated flow-induced dilation (FID) and hypoxia-induced dilation (HID) in the presence or absence of A1R/A2aR agonists (CCPA and CGS-21680, respectively) and antagonists (DPCPX and SCH-58261, respectively) in isolated middle cerebral arteries (MCAs) from Sprague Dawley rats of both sexes and the direct dose-dependent effects of A1R and A2aR agonists on the vascular reactivity of MCAs. Rats were exposed to either acute HBO₂ (Ac-HBO₂) or intermittent HBO₂ over four days (In-HBO₂). Ac-HBO₂ impaired vascular responses to A1R and A2aR agonists and significantly decreased FID and HID. In both Ac-HBO₂ and In-HBO₂, A1R modulation did not significantly affect FID or HID. A2aR stimulation reduced FID in the In-HBO₂ group, while A2aR antagonism had no significant effect on HID. However, the A2aR agonist’s presence enhanced HID in In-HBO₂-exposed rats. Protein expression of A1R and A2aR decreased after Ac-HBO₂, while gene expression increased following In-HBO₂. These findings suggest that ARs play a role in HBO₂-induced vasoreactivity, which possibly changes in MCA, potentially via the modulation of ARs gene and protein expression.

The kidneys play an important role in controlling arterial blood pressure by regulating extracellular fluid volume, through excretion of sodium and water, which is called pressure natriuresis, or diuresis. Sodium and water homeostasis is controlled by the integrated physiological functions of organ systems, including renal mechanisms, but also with an influence of the renal and non-renal sympathetic nervous system and the endocrine system (renin-angiotensin-aldosterone system, cardiac natriuretic peptides, antidiuretic hormone, and oxytocin). Pressure natriuresis represents the basal level for arterial blood pressure dysregulation. The imbalance of complex renal and non-renal hemodynamic and neurohumoral mechanisms leads to the disruption of antidiuretic mechanisms, which results in the development of arterial hypertension. Knowledge of all mechanisms enables an integrated understanding of the regulation of arterial blood pressure, which is a key step in the targeted and individual treatment of one of the most common diseases today.