Despite intensive research, the exact cause of hypertension remains unknown. Low-grade inflammation has been proposed to play a key role in the pathogenesis of hypertension. Both innate and adaptive immune responses may participate in this process. Several studies have addressed the contribution of adaptive immunity to the pathophysiology of high blood pressure; however, the role of innate immunity is less clear. Innate immunity may be an important mediator of chronic inflammation in hypertension. Slight elevation of blood pressure due to increased sympathetic and/or decreased parasympathetic outflow, or low-grade infections may generate neoantigens and damage-activated molecular patterns (DAMPs) or pathogen-activated molecular patterns (PAMPs), which can trigger Toll-like receptors on innate effector cells. Innate responses, mediated by monocytes, macrophages, dendritic cells and natural killer cells, may contribute to inflammation either directly or by activating adaptive immune responses mediated by T lymphocytes. In this review, we discuss the recent evidence regarding the contribution of different innate effector cells, their response and their mechanisms of activation in hypertension.