The adverse effects of plastics on the environment, wildlife, and human health have been extensively studied, yet their production remains unavoidable due to the lack of viable alternatives. Environmental fragmentation of larger plastic particles generates microplastics (MPs, 0.1-5000 μm) and nanoplastics (NPs, 1-100 nm), which can enter the bloodstream through inhalation or ingestion. This review examines whether MPs and NPs influence blood pressure. To address this question, relevant studies were analyzed based on predefined criteria. Due to anatomical barriers and microcirculatory dynamics, only NPs and small MPs are expected to enter the bloodstream under physiological conditions, although pathological states may alter this. In vitro research indicates that MPs and NPs negatively affect erythrocytes and endothelial cells, while rodent models suggest potential cardiovascular effects. Plastic particles and fibers have been detected in human blood, thrombi, atherosclerotic plaques, and various tissues. However, validated data on plastic particle-related blood pressure changes remain lacking. Despite limitations in their applicability to human physiology, preclinical models suggest that MPs and NPs circulate in the bloodstream, interact with blood cells, and contribute to vascular damage. Mechanisms such as endothelial injury, platelet activation, inflammation, and MPs/NPs accumulation in atherosclerotic plaques may contribute to blood pressure elevation but are unlikely to be the exclusive cause of hypertension. Further research is needed to clarify the role of plastic particles in blood pressure regulation. Standardized detection methods, real-world scenario-related models, and targeted human studies are essential to assessing cardiovascular risks associated with MP and NP exposure.