Autonomic Regulation of Cardiovascular Function in Health and Disease MEETING PROGRAM AND ABSTRACTS

s of Invited and Contributed Presentations 1.0 Plenary Lecture I....................................................................................12 2.0 Angiotensin Converting Enzyme 2 and ANG (1-7): Roles in Central Hypertension.....12 3.0 Poster Session I....................................................................................12 4.0 Oxidative Stress and Sympathetic Regulation..................................................16 5.0 Mechanisms of Baro and Chemoreceptors Sensory Transduction: A Link to Sympatho-excitation in Disease..................................................................17 6.0 Plenary Lecture II...................................................................................17 7.0 Sympatho-excitatory Mechanisms in Cardiovascular Disease.................................17 8.0 Poster Session II....................................................................................18 9.0 Sympathetic Mechanisms in Human Hypertension............................................21 11.0 Plenary Lecture III.................................................................................21 12.0 Nitric Oxide and Sympatho-vagalregulation....................................................21 13.0 Poster Session III...................................................................................22 14.0 Device Therapy for Hypertension and Heart Failure..........................................24 Author Index.................................................................................................27 2012 APS Conference: Autonomic Regulation of Cardiovascular Function in Health & Disease ABSTRACTS OF INVITED AND VOLUNTEERED PRESENTATIONS 12 1.0: PLENARY LECTURE I 1.1 ADVANCES IN THE CENTRAL RENIN-ANGIOTENSIN SYSTEM Curt Sigmund 1 The renin-angiotensin system (RAS) in the brain is well recognized as an important controller of cardiovascular (CV) function though its effects on blood pressure (BP), fluid intake, and sympathetic outflow, and has been implicated in hypertension. Growing evidence advancing the concept that the RAS, both in the brain and periphery, is also a controller of energy expenditure is gaining acceptance. We have obtained compelling data indicating that activation of the brain RAS, while simultaneously decreasing circulating RAS, results in increased energy expenditure. These data advance the novel concept that the central and peripheral RAS may differentially control energy balance. Moreover, our most recent data suggest a novel role for adipose AT Pharmacology, Univ. of Iowa, 2-454 BSB, Iowa City, IA, 52242. 2R as a modulator of the actions of the brain RAS on adipose tissue and its resulting effect on energy expenditure. Activation of adipose AT2 R blunts energy expenditure induced in response to elevated brain RAS activity. Activation of the brain RAS also increases BP and fluid intake through efferent mechanisms distinct from those controlling energy expenditure. This plenary lecture will review the central pathways regulating ANGII synthesis, the role of renin in the brain, the contrasting mechanisms regulating cardiovascular and metabolic output of the brain RAS, and the interaction between the RAS in the brain and adipose tissue and its effects on energy balance. This work was funded by grants from the NIH, AHA, and the Roy J Carver Trust. 2.0: ANGIOTENSIN CONVERTING ENZYME 2 AND ANG (1-7): ROLES IN CENTRAL HYPERTENSION 2.1 BRAIN ANGIOTENSIN PEPTIDES AND CONTROL OF BLOOD PRESSURE Debra Diz 1 Alterations in autonomic outflow contribute to both cardiovascular and metabolic changes accompanying hypertension and aging. Investigation of our hypothesis that angiotensin (Ang) II and Ang-(1-7) in dorsal medullary nuclei favor activation of the sympathetic vs. parasympathetic systems, respectively, reveals divergent actions of the peptides on resting mean arterial pressure (MAP), baroreflex sensitivity for control of heart rate (BRS) and indices of metabolic function. Our studies further identify different anatomical, neurotransmitter and signaling pathways involved as potential mechanisms for the distinct actions of the peptides. Examples illustrating these concepts will be drawn from models of aging, as well as acute and chronic elevations of MAP in stress, fetal-programming and genetic hypertension. The influence of long-term alterations in medullary angiotensin peptides on cardiovascular responses to activation of nTS receptors for cardiometabolic hormones/transmitters such as leptin and CB1 endocannibinoids, and to differences in resting levels of local transmitters known to be involved in BRS, will be highlighted using data from transgenic animals. The functional interactions between the renin-angiotensin system (RAS) and the autonomic nervous system in brain and periphery illustrated in our studies continue to provide strong rationale for therapeutic interventions involving RAS blockade for cardiometabolic protection. The emerging new concept is that both reduced Ang II and elevated Ang-(1-7) may be required for optimal benefit over the long-term. (HL51952, HD474584). Hypertension & Vascular Res. Ctr., Wake Forest Sch. of Med., 1 Medical Ctr. Blvd., Winston-Salem, NC, 27157-1032. 2.2 ACE2 REGULATION IN HYPERTENSION