The autonomic nervous control of cardiovascular (CV) system plays a major role in the adaptation of the organism to the changes in external and internal environment. It’s dysfunction is the major pathophysiological factor in the development of neurocardiovascular diseases. The aim of this review is to present the state of the art on the role of candidate gene polymorphisms of the molecules in the signaling chain of neurocardiovascular transmission in neurocardiovascular diseases. Neurocardiovascular disorders can be classified as sympathetic vs. vagally mediated disorders, though in many disorders both systems are dysfunctional. A number of molecules along the signaling pathway can be functionally modified and be the background of the predisposition, faster progression or complicated form of the disease. When the disease is the consequence of the joined parasympathetic and sympathetic nervous system disequilibrium, the focus of neurogenetic research should be on molecules providing the cross-talk between the two systems: on intercellular and intracellular level and on the level of the signaling process integration. An aggregation of positive results for the association between certain genes and different neurocardiovascular phenotypes pointed on a specific "neurocardiovascular genetic hotspots". Identification of these genes could be of particular interest as a diagnostic tool in the clustered form of neurocardiovascular diseases. New data obtained from neurogenetic approach will improve the disease outcome by gene, pharmacologic and behavioral modulation of the autonomic nervous system.