Brief Reviews Autonomic Neural Regulation of the Immune System Implications for Hypertension and Cardiovascular Disease

The autonomic and the immune systems play major rolesin the pathogenesis of cardiovascular disease and hyper-tension. To date, those 2 systems have been studied exten-sively but independently by cardiovascular biologists and by immunologists. The notion that the autonomic system can modulate the immune system and thereby influence the pathogenesis of cardiovascular disease and hypertension and their clinical outcome is novel and critical. In this brief review we focus on that interaction and an integrated understanding of the neuro-immune axis. We also highlight recent progress and future research directions. The main theme is that dysregulation of the autonomic system enhances the inflammatory response of the innate and adaptive immune systems leading to the initiation or accel-eration of pathological processes and worsening of cardio-vascular risks. The therapeutic potential of restoring an optimal autonomic control of the immune system is very promising. Both components of the neuro-immune axis may be in-volved in its disruption. One is the autonomic nervous system, which may be dysregulated or imbalanced with increased sympathetic and decreased parasympathetic activa-tion. The other is the immune system itself, which may be abnormally sensitive to the modulatory influence of the autonomic system. These 2 components are briefly described below. Autonomic Dysregulation in Chronic Hypertension The complexity of cardiovascular mechanisms that contribute to hypertension has been challenging. The roles of vascular and renal abnormalities are undeniable. Changes in vasomo-tor tone, sodium retention, and renal renin release are all well established. For decades the contribution of the sympathetic nervous system to chronic hypertension was not fully appre-ciated. Its importance is now well recognized.1–5 In a 1982 review, we described the neural sites and mechanisms in-volved in exaggerated sympathetic nerve activity (SNA) in several animal models, as well as in human hypertension.1 Moreover, there has been a surge of data highlighting the damaging cardiovascular effects and the increased mortality and morbidity associated with exaggerated SNA in a variety of cardiovascular diseases.6–10 In the Cannon Lecture of 200