Autonomic Regulation of Cardiovascular Function in Health and Disease

Over the past 100 years we have acquired a fairly comprehensive understanding of the neural mechanisms that regulate arterial pressure and peripheral resistance. In the past 20 years we have elucidated many cellular and molecular mechanisms that control sympathetic nerve activity. Much of the work has been driven by a lack of understanding of the mechanisms responsible for the development of essential hypertension.

There is little doubt that augmented sympathetic nerve activity contributes to the pathogenesis of a variety of disease states including hypertension, heart failure, diabetes and panic disorders. We now have the capability to understand discrete molecular mechanisms responsible for altering sympathetic nerve activity in disease states. These mechanisms alter specific ion channel function and membrane properties in order to evoke sympatho-excitation.

The conference will focus on many of these mechanisms. Sessions will include the role of the autocrine, paracrine and endocrine mediators in reflexes and areas of the central nervous system that are known to regulate sympathetic function (e.g. the hypothalamus and medulla). Symposia and poster abstracts will focus on reactive oxidant stress, nitric oxide, angiotensin II, angiotensin (1-7), glutamate, GABA and the transcriptional and translational regulation of the receptors for many of these mediators. An important component of this conference will be several sessions on neural mechanisms that mediate sympatho-excitation in hypertension, heart failure, diabetes and panic disorders. These sessions will include talks on studies carried out in both animals and humans. It will be critical to incorporate sessions on human autonomic physiology in order to explore the potential for translational aspects of experimental findings.