Vagal-Immune Interactions in the Control of Hypertension

There is a consensus in the literature that the autonomic dysfunction in arterial hypertension involves the increase of sympathetic activity and, also, reduction of vagal tone. In the last years, the role played by inflammation in the development of hypertension and target organs injuries, such as heart and blood vessels, has been emphasized. Although the clinical importance of sympathetic hyperactivity and its treatment of arterial hypertension is recognized, the therapeutic benefit of increasing parasympathetic activity in hypertensive patients still requires an in-depth investigation. The increased vagal activity may produce beneficial effects on cardiovascular modulation and inflammation, preventing target organ damage. Parasympathetic neurotransmission can be improved by the inhibition of acetylcholinesterase action. Anticholinesterase agents prevent the hydrolysis of acetylcholine by acetylcholinesterase, prolonging its availability within the cholinergic cleft. This article will highlight the key concepts of the cardiac autonomic imbalance and the increase of acetylcholine availability under inflammation and control of arterial hypertension. In conclusion, significant evidence exists associating the reduction of parasympathetic activity and the occurrence of inflammation involving the pathophysiology of hypertension; suggesting that the improvement of vagal activity by the increased availability of acetylcholine has a remarkable potential for the therapeutic intervention on arterial hypertension.