Cellular mechanism of cardio-adrenal interaction

点击翻译按钮获取中文摘要

Chronic salt overload in Dahl-salt sensitive rats stimulates aldosterone production via local activation of renin-angiotensin system (RAS). Beta3-adrenergic receptor was highly upregulated concomitant with the progression of cardio-renal injury. Adrenal glands became hypoxic as cardio-renal injury progress and both hypoxia induced the expression of beta3-adrenergic receptor via HIF activation in adrenocortical cells. Macrophages were infiltrated in the adrenal cortex in rats with cardio-renal injury and macrophage ablation reduced aldosterone production. Co-culture with macrophages or a supernatant of macrophages stimulated CYP11B2 expression in adrenocortical cells. Acquisition of catecholamine-responsiveness via the induction of beta3-adrenergic receptor under tissue ischemic and crosstalk between macrophages and adrenocortical cells accounts for the RAS-independent aldosterone production associated with cardio-renal injury.