Sympathetic nervous system overactivity and its role in the development of cardiovascular disease.
This review examines how the sympathetic nervous system plays a major role in the regulation of cardiovascular function over multiple time scales. This is achieved through differential regulation of sympathetic outflow to a variety of organs. This differential control is a product of the topographical organization of the central nervous system and a myriad of afferent inputs. Together this organization produces sympathetic responses tailored to match stimuli. The long-term control of sympathetic nerve activity (SNA) is an area of considerable interest and involves a variety of mediators acting in a quite distinct fashion. These mediators include arterial baroreflexes, angiotensin II, blood volume and osmolarity, and a host of humoral factors. A key feature of many cardiovascular diseases is increased SNA. However, rather than there being a generalized increase in SNA, it is organ specific, in particular to the heart and kidneys. These increases in regional SNA are associated with increased mortality. Understanding the regulation of organ-specific SNA is likely to offer new targets for drug therapy. There is a need for the research community to develop better animal models and technologies that reflect the disease progression seen in humans. A particular focus is required on models in which SNA is chronically elevated.
Malpas
Simon C
SC
Department of Physiology and the Auckland Bioengineering Institute, University of Auckland and Telemetry Research Ltd., Auckland, New Zealand. s.malpas@auckland.ac.nz
D000818:Animals; D002317:Cardiovascular Agents / Q000494:pharmacology*; D006331:Heart Diseases / Q000188:drug therapy / Q000503:physiopathology*; D006801:Humans; D006973:Hypertension / Q000188:drug therapy / Q000503:physiopathology*; D013564:Sympathetic Nervous System / Q000503:physiopathology*
D002317:Cardiovascular Agents