Pharmacological Modulation of Vagal Nerve Activity in Cardiovascular Diseases

Figures

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  Fig. 1. Methods and indices used to evaluate vagal activity in cardiovascular disease. Vagus activity can be evaluated by (I) measurement of the vagal discharge (image adapted from Lu Y et al. [27]); (II) autonomic tone and intrinsic heart rate; (III) HRV and BRS; (IV) cardiac autonomic nerves and cholinergic nerve distribution; and (V) detection of the release of ACh into the circulation (image adapted from Zhao M et al. [6]). ACh, acetylcholine; BRS, baroreflex sensitivity; HPLC, high performance liquid chromatography; HRV, heart rate variability; PSYM, parasympathetic; SYM, sympathetic.

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  Fig. 2. Schematic of the drug targets for vagal nerve activation. A The vagal transmitter ACh is synthesized in vivo by the catalysis of choline and acetyl-CoA by choline acetyltransferase, thus directly increasing the levels of synaptic ACh [67]. B Cholinesterase inhibitors increase the levels of synaptic ACh by decreasing its degradation, and thus directly increasing vagal tone [68]. C Adenosine [69], statins [70], beta-receptor blockers [71], and ACEIs [72] indirectly activate vagal tone by acting on the related receptors. Acetyl-CoA, Acetyl-coenzyme A; AChE, acetylcholine esterase; ACEIs, angiotensin-converting-enzyme inhibitors; ACh, acetylcholine.