Regulation of human salt-sensitivite hypertension by myeloid cell renin-angiotensin-aldosterone system

Introduction: Salt sensitivity of blood pressure is a phenomenon in which changes according to dietary sodium intake. Our previous studies found that high salt activates antigen presenting cells, resulting the development hypertension. The mechanisms by salt-induced immune cell activation regulated are unknown. In current study, we investigated effects on renin-angiotensin-aldosterone system (RAAS) gene expression myeloid cells and their impact sensitive hypertension humans. Methods: We performed both bulk single-cell sequencing analysis with vitro vivo treatment humans using rigorous salt-loading/depletion protocol phenotype salt-sensitivity pressure. also measured plasma renin aldosterone radioimmunoassay. Results: while exposure downregulated renin, binding protein receptor, there were no significant genes renin-angiotensin response loading depletion . Plasma individuals tended be lower blunted loading/depletion challenge as previously reported. Discussion: These findings suggest unlike systemic RAAS, acute intake do not regulate RAAS cells.