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Review
. 2012 Apr;59(4):755-62.
doi: 10.1161/HYPERTENSIONAHA.111.186833. Epub 2012 Feb 13.

Autonomic neural regulation of the immune system: implications for hypertension and cardiovascular disease

François M Abboud  1 , Sailesh C Harwani, Mark W Chapleau
Affiliations
Review

Autonomic neural regulation of the immune system: implications for hypertension and cardiovascular disease

François M Abboud et al. Hypertension. 2012 Apr.
No abstract available

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Figures

Figure 1
Figure 1
Mechanisms involved in excessive sympathetic activity and reduced parasympathetic activity in cardiovascular disease. This dysautonomia is associated with increased morbidity and mortality [11].
Figure 2
Figure 2
The triangle reflects the convergence of the neural and immunological mechanisms in cardiovascular disease. It can be either a “Death Triangle” with excessive sympathetic and RAAS activities that enhance the inflammatory immune response and increase mortality, or a “Survival Triangle” with enhanced parasympathetic activity which has been shown to suppress the inflammatory immune response and prolong survival.
Figure 3
Figure 3
Centrally-driven increase in splenic sympathetic nerve discharge (SND) by Ang II infusions (ICV) induces a marked increase in splenic gene expression of several cytokines. Selective splenic denervation abrogates the responses while the increase in renal SND is preserved. Adapted from Ganta et al. [48].
Figure 4
Figure 4
A: Subdiaphragmatic vagotomy induces pronounced NFκB-activation in the colon in vivo over a period of 4 weeks (w) post-vagotomy. Adapted from Omahony et al. [49]. B: Vagotomy results in a significant increase in gene expression of IFNγ, TNF, and IL-6 in isolated splenic murine CD4+T lymphocytes. Adapted from Karimi et al. [50].
Figure 5
Figure 5
The autonomic, neurohumoral sympathetic and vagal signals regulate both the innate and adaptive immune cells. The activation of cholinergic (nAChR), adrenergic (α/β ADR) or angiotensin receptors (AT1R) on innate cells may dramatically alter the TLR-mediated cytokine release in pathologic states such as hypertension [43]. This, in turn, activates the adaptive cytotoxic T-lymphocytes, which cause end-organ damage in blood vessels and kidney. [42, 44, 60].
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