Inappropriate mineralocorticoid receptor (MR) activation in monocytes/macrophages promotes cardiac inflammation and fibrosis. However, the specific pathways whereby the MR regulates macrophage phenotype are not fully defined. We recently identified bidirectional regulation of the MR and the molecular circadian clock in cardiac cells. Given that immune cells are important regulators of cardiac pathology, we investigated whether MR regulates the molecular circadian clock and time of day expression of inflammatory mediators in splenic monocytes/macrophages using myeloid MR null mice (MyMRKO). RNAseq and RT-qPCR analysis of whole spleen from floxed control (FC) or MyMRKO revealed differential expression of clock genes Per2, Cry1, REV-ERBα, and DBP at (Zeitgeber time) ZT0 versus ZT12. Time-of-day regulation of numerous gene targets were also disordered in MyMRKO spleen versus FC including NOS2, CXCR4, FABP3, S100A8, S100A9 and FGF1. Aldosterone induction of REV-ERBα, Cry1, iNOS, IL-1β, Arg-1, IL-10, CCL2 and Spp1 was greater when delivered at ZT0 vs ZT12, when corticosterone levels are low. Moreover, oscillating expression of Per2, REV-ERBα and other clock components was regulated by 10nM aldosterone or corticosterone in immortalised bone marrow derived cells, supporting a direct role for MR modulation of cellular clock time. Significant differences observed between male and female samples underscore the role of sex in the modulation of circadian signalling and MR dependent proinflammatory phenotype in myeloid cells. Cardiac macrophage-specific bulk RNAseq and scRNAseq datasets verified MR-dependent regulation of many temporally induced genes in immune cell subsets, whereas FACS analysis showed immune cell populations were mostly unchanged and that IL-1β expression is highest in myeloid cells consistent with MyMRKO regulating IL-1 β in this population. Our findings demonstrate the dynamic influence of MR transcriptional control of circadian clock and inflammatory pathways in myeloid cells, highlighting potential sex-based differences and offering insights into potential mechanisms underpinning MR modulation of myeloid cell phenotype.