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The mineralocorticoid receptor (MR) is present in a myriad of extrarenal tissues, including endothelial cells,1 vascular smooth muscle cells, and cardiac myocytes.2 The physiological role played by the MR in these tissues remains unclear because, as yet, aldosterone seems to have only deleterious effects at these receptors. The study by Rickard et al3 adds macrophages to the list of cells where aldosterone has pathophysiological effects. This group has shown that aldosterone, or MR activation, is intrinsically involved in cardiac fibrosis and that inflammation and macrophage infiltration are precursors to this.4,5 The latest article highlights the importance of macrophages in this process and assigns a key role to the MR in macrophages (Figure). This elegant study used macrophage-specific MR knockout mice. When treated with deoxycorticosterone (DOC), wild-type mice develop hypertension, cardiac fibrosis, and inflammation concomitant to macrophage infiltration. Knockout mice show macrophage infiltration but do not develop fibrosis or hypertension. This tells us 2 things. First, macrophages may infiltrate a tissue without having detrimental effects. Second, the macrophage MR is needed to mediate the blood pressure and fibrogenic responses but not for infiltration. Figure. Macrophage-specific deletion of the MR does not impair adhesion or infiltration in response to DOC but does prevent the formation of cardiac fibrosis.That is only one side of the story. The role played by aldosterone in the inflammatory response becomes complicated when one considers the infiltration process. The study by Rickard et al3 suggests the macrophage MR does little to control infiltration. However, studies by Caprio et al1 suggest that …

Are Macrophages the Foot Soldiers in the War Waged by Aldosterone Against the Heart?