Finally, protein kinase D (PKD)-1 activation leading to cardiac hypertrophy has also been linked to the MR-EGFR crosstalk in aldosterone-treated cardiac myocytes [80], whereas, in vascular endothelial cells, aldosterone enhances nitric oxide production via MR- and phosphoinositol 3-kinase (PI3K)-dependent endothelial nitric oxide synthase (eNOS) phosphorylation [81]. This evidence concerns the gene NR3C2 and cardiac hypertrophy.