Renal Myeloid Mechanisms, Cross‐Talk in Hypertension

Hypertension involves an impairment of renal sodium excretion along with activation of pro-inflammatory responses in the kidney. Dendritic cells (DCs) are professional antigen-presenting cells that sense disturbances in cell and tissue homeostasis to orchestrate T cell activation and recruitment. Renal DCs distribute as a cellular network throughout the renal interstitium, forming an interface between innate and adaptive immunity. Here, we explore what is known about renal cross-talk following prohypertensive stimuli, which modify renal DCs, T cell polarization, and renal function, leading to hypertension. We also present the phenotypic and functional heterogeneity of DCs, including literature on in vitro and in vivo signaling mechanisms in a variety of hypertensive models. Current studies indicate that renal sodium retention caused by prohypertensive stimuli requires DC function. The prohypertensive action of DCs also requires T cell function. Several cross-talk mechanisms have been proposed, such as signals from the kidney to the DC, including salt activation of DC's via RAAS receptor signaling, and DC-dependent recruitment of T cells to the kidney then promoting increased renal tubular sodium reabsorption. Knowledge gaps include specific functions of renal DC subtypes, sex differences in DC-mediated hypertension, and clinical studies on DC function in hypertension. The identification of mechanisms leading to renal DCs activation in hypertension may offer new strategies for the prevention and treatment of hypertension.