Activation of the mineralocorticoid receptor (MR) in the distal nephron by its ligand, aldosterone, plays an important role in sodium reabsorption and blood pressure regulation. However, expression of the MR goes beyond the kidney. It is expressed in a variety of other tissues in which its activation could lead to tissue injury. Indeed, MR activation in the cardiovascular (CV) system has been shown to promote hypertension, fibrosis, and inflammation. Pharmacological blockade of the MR has protective effects in several animal models of CV disease. Furthermore, the use of MR antagonists is beneficial for heart failure patients, preventing mortality and morbidity. A better understanding of the implications of the MR in the setting of CV diseases is critical for refining treatments and improving patient care. The mechanisms involved in the deleterious effects of MR activation are complex and include oxidative stress, inflammation, and fibrosis. This review will discuss the pathological role of the MR in the CV system and the major mechanisms underlying it.