Systemic considerations autonomic nervous system

In this hypothetical mechanistic scheme, it is postulated that electrocardiographic alterations produced by exposure to air pollutants will result partly from central nervous system (CNS)-mediated changes in cardiac autonomic tone. This supposition is based on the fact that the main cytokines that are released in response to air pollution can alter CNS activity. Also subjecting the lungs to noxious stimuli may elicit powerful cardiac reflexes that can alter sympathetic and parasympathetic activity. This is a critical consideration, because it is well established that both divisions of the autonomic nervous system exert a profound influence on the repolarization properties of the heart. These potential changes may play a vital role in the culminative response of inhaled particles on the cardiopulmonary system. 

There is considerable diversity among nicotinic acetylcholine receptors, and at least one source of this diversity is the multiplicity of acetylcholine receptor genes. Cholinergic-nicotinic receptors in skeletal muscle are different from those in autonomic ganglia and the central nervous system. 

Interest in substance P in modulating autonomic reflexes in the NTS has waxed and waned over the past several years (Helke and Seagard 2004). The neuropeptide is widely distributed throughout the peripheral nervous system and the CNS. There are considerable data on the role of the neuropeptide as a neuromodulator it has been proposed to play a role in asthma, cough and other respiratory reflexes, emesis, psoriasis, and a number of neuropsychiatric disorders. Attempts to develop therapeutic agents have been somewhat disappointing - which may reflect the complexity of the effects of substance P in the CNS. 

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