Autonomic nervous system control of the cardiovascular and respiratory systems in asthma

Abstract

Patients with asthma have exaggerated bronchoconstriction of their airways in response to certain indirect (e.g. cold air, allergens, dust, exercise) or direct (e.g. inhaled methacholine) stimuli. This 'hyper-reactivity' usually co-exists with airway inflammation, although the pathophysiological mechanisms underlying these changes are not fully understood. It is likely that this hyper-reactivity is associated with abnormal autonomic nervous system (ANS) control. In particular, the parasympathetic (vagal) component of the ANS appears to be implicated in the pathogenesis of asthma. In addition, several studies have suggested the existence of differential alteration in ANS function following exercise in asthmatics compared with non-asthmatic individuals. Several early studies suggested that the altered autonomic control of airway calibre in asthma might be reflected by a parallel change in heart rate. Cardiac vagal reactivity does indeed appear to be increased in asthma, as demonstrated by the cardiac response to various autonomic functions tests. However, other studies have reported a lack of association between bronchial and cardiac vagal tone, and this is in accord with the concept of system-independent ANS control. This review provides a discussion of cardiovascular-autonomic changes associated with either the pathophysiology of asthma per se or with asthma pharmacotherapy treatment. Previous investigations are summarised suggesting an apparent association between altered autonomic-cardiovascular control and bronchial asthma. The full extent of autonomic dysfunction, and its clinical implications, has yet to be fully determined and should be the subject of future investigation.

Do asthma patients with panic disorder really have worse asthma? A comparison of physiological and psychological responses to a methacholine challenge

“…Methacholine is known to produce bronchoconstriction of the airways [57], which is thought to be driven by parasympathetic activation [58,59]. Methacholine has also been shown to lower blood pressure [60], so it is plausible that a methacholine-induced imbalance between parasympathetic and sympathetic tone could explain our results of diminished physiological responses in reaction to the MCT.…”

Neuropeptides Activate Human Mast Cell Degranulation and Chemokine Production

“…Such an effect could contribute to airway hyperreactivity such as occurs in asthma. 62 We found that VIP and SP, but not NGF or CGRP, caused human mast cells to produce chemokines such as RANTES and MCP-1, suggesting that these mediators may be involved in neurogenic inflammation. Injections of RANTES in the skin of humans and of rats caused eosinophil and macrophage recruitment.…”

Human Movement Control

“…A reflex response occurs when there is a change in the blood pressure or the chemistry within the body. This makes the cardiovascular centre to stimulate or inhibit the cardioacceleratory centre, the cardioinhibitory centre and the vasomotor centre until equilibrium or homeostasis is reached [10] (Figure 3). …”