The data suggesting that hyperprolactinemia results in higher circulating vasoinhibin levels which, in turn, induce plasminogen activator inhibitor-1 expression, lower eNOS phosphorylation/activation, and reduce nitric oxide production are novel, and they complement information regarding endocrine circuits in the prolactin/vasoinhibin axis and their relevance for cardiovascular function (3). This evidence concerns the gene PRL and hyperprolactinemia.