Interrupting neural pathways that transduce stressful information into physiological responses

Abstract

Stressor-stimuli evoke a noradrenergic process in the frontal lobes, the amplitude of which depends on both the individual's experience with the stimulus and his or her genetic background. Novel and noxious stimuli evoke large frontocortical responses and benign ones evoke relatively larger reactions in persons with a family history of cardiovascular disease. Blockade of neural projections from the frontal cortex and amygdala to the brainstem cardiovascular centers will normalize blood-pressure elevations in experimental hypertension and prevent lethal arrhythmias in animals with a myocardial infarction. The anti-mortality effect of the cardiac drugs known as beta-blockers is exerted by inhibition of cerebral beta-receptors, not peripheral ones. A new putative neuropeptide, NLX, may have the same desirable cardiovascular effects, but without the side-effects that limit clinical usefulness. The neural regulation of the heart during stress can be detected by a new deterministic measure of low-dimensional chaos in heartbeat intervals. In both animals and humans undergoing myocardial infarction, this deterministic measure correctly predicts lethal arrhythmogenesis, minutes to hours prior to the event. Thus an approach combining both brain and heart studies (i.e., "neurocardiology") has led to an understanding of how stressor-stimuli evoke autonomic reactions. This, in turn, has led to new methods in the diagnosis and treatment of cardiovascular disorders.