Independent Learning Module: The Biological Basis of Cardiovascular Reactivity
A focal point of psychosomatic research has examined the pathogenic influence of psychological stress on physical health. In particular, augmented cardiovascular reactivity to acute psychological stress has received considerable attention due to its association with prospective adverse cardiovascular outcomes. However, the precise mechanism by which psychological stress perturbs the cardiovascular system is often poorly understood. As a PhD student researching in the field of cardiovascular psychophysiology, I am fascinated with the idea that psychological perceptions and interpretations of stressful stimuli can alter cardiovascular activity.
However, as I commenced researching in the area, I began to continually question how psychological perceptions can influence cardiovascular parameters. How can a perception and a current state of thinking modify physiological functioning?
In order to acquire answers to the above questions and enhance my understanding of the topic, I completed an independent learning module. Synthesised information from the manuscript is summarised below.
So how does stress perturb cardiovascular activity?
The appraisal of the stressor involves a number brain structures including the limbic system and the prefrontal cortex. Together these areas form a cognitive emotional response to the stressful stimulus encapsulating evaluations, perceptions and affective responses. These subjective perception and interpretations are transformed into autonomic and endocrine outputs by the hypothalamus and brain stem. The sympathetic nervous system is the most crucial mechanism in the stress response. Sympathetic activation again begins at the hypothalamus where neurons extend to areas of the brainstem responsible for descending activation through the central nervous system. The autonomic nerve pathway extends from the central nervous system to the effector organs via two neuron chains, preganglionic and postganglionic nerve fibres. The sympathetic nerve fibres in the central nervous system are referred to as preganglionic fibres and originate in the lumbar and theoretic regions of the spinal cord. These preganglionic fibres synapse with postganglionic fibres within autonomic ganglia, located in the sympathetic trunk at either side of the spinal column. Postganglionic fibres originate in these autonomic ganglia and end at effector organs (e.g the heart). Action potentials descending down the spinal cord cause nerve impulses in preganglionic fibres, engendering the release of the neurotransmitter acetylcholine (Ach) into synapses located in autonomic ganglia. Once released, acetylcholine crosses the synapses and stimulates action potentials in the postsynaptic postganglionic fibres. The postganglionic fibres then carry the action potential to the effector organ, where the neurotransmitter norepinephrine is released into the synapse, causing a response in the effector organ (e.g. heart and blood vessels) (See figure 1).
In addition to neural activation of effector organs, the sympathetic nervous system also stimulate hormonal secretion via the adrenal medulla. Some preganglionic sympathetic nerve fibres originating in the central nervous system project to the inner portion of the adrenal glands located just above the kidneys (adrenal medulla). However, the adrenal medulla does not give rise to any postganglionic fibres, instead it secretes hormones into the bloodstream (See figure 2). The adrenal medulla is responsible for the secretion of two stress hormones including epinephrine and norepinephrine. As noted above, norepinephrine is a neurotransmitter released by postganglionic sympathetic fibres and causes a response at an effector organ. However, when produced by endocrine glands, such as the adrenal medulla and released into the bloodstream, norepinephrine and its sister molecule epinephrine are considered hormones. Although, norepinephrine can be expressed as both a neurotransmitter and a hormone, it has precisely the same influence on effector organs. Finally, norepinephrine and epinephrine then cause a response in effector organs by binding to adrenergic receptors, similar to a lock and key.
