Excessive Sympathetic Nervous System Output Is Detrimental to Health

Stimulation of the SNS is a hallmark of the acute stress response (Goldstein, 1987). SNS activation has many physiological consequences that work in concert to promote the fight-or-flight response (Jansen et al., 1995; Goldstein, 1996) and facilitate features of innate immunity (Campisi and Fleshner, 2003; Johnson et al., 2005). SNS activation is a powerful feature of the acute stress response that is adaptive when the response is acute and constrained. If, however, SNS activation is frequent or excessive, it can produce negative health consequences (Seals and Dinenno, 2004). For example, chronically elevated SNS responses are believed to mechanistically contribute to the etiology of "metabolic syndrome," a key antecedent to clinical atherosclerotic diseases that includes visceral adiposity, glucose intolerance, insulin resistance, dyslipidemia, and hypertension (Baron, 1990; Julius et al., 1992; Lind and Lithell, 1993). In addition, it has been reported in both the human and animal literatures that chronic or excessive SNS activation can lead to arterial wall thickening (Pauletto et al., 1991; Chen et al., 1995; Xin et al., 1997), hypertension (Lind and Lithell, 1993), a- and ß-adrenergic receptor desensitization (Abrass, 1986; Xiao and Lakatta, 1992; Dinenno et al., 2002), and immunosuppression (Irwin, 1993; Kennedy et al., 2005b). The negative consequences of frequent and/or excessive SNS activity have been convincingly demonstrated in transgenic mice lacking functional a2A adrenergic receptor (ADR) autoinhibition in the midbrain. Due to the lack of normal a2AADR central nervous constraint on SNS drive, these mice have chronically activated peripheral SNS responses and rapidly develop cardiac dysfunction (Baum et al., 2002). Unfortunately, neither tissue NE nor immune function was assessed in this study.

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