Model Components

Stressor/Hooks(s): Internal and/or external events that can be acute, episodic, or chronic in nature.

Thoughts: Beliefs and perceptions regarding those events.

Distortions, or "hot thoughts," have the potential to increase arousal.

Self-Esteem: A realistic, appreciative opinion of oneself, resulting from unconditional love, worth, and growth.

Research and/or clinical experience support a relationship between low self-esteem and manifestations of physical and mental illness, such as physical and emotional abuse, drug abuse, and the like. The feedback loop in the model suggests that emotional and behavioral states may further erode self-esteem.

Core Belief(s): Underlying beliefs (e.g., people are bad and inept, and shouldn't be; I'm a person, therefore I'm inept) and expectations that may be unrealistic can result in distorted cognitions.

Anger: The emotion resulting from the thoughts.

Behavior(s): Voluntary actions that follow from and influence an individual's emotions. Disproportionate anger may contribute to unhealthy behaviors such as a sedentary lifestyle, poor nutrition, drug abuse, delinquency, and the like.

Hypothalamus-. A part of the brain that organizes the "fight or flight" response.

Primary Stress Response Pathways

A represents the immediate pathway—direct innervation of organs by the sympathetic branch (SNS) of the autonomic nervous system. This pathway is the fastest acting pathway, given the capability of nerves to transmit messages rapidly. The immediate effects of direct organ innervation are:

• Increased heart rate, stroke volume, and, therefore, cardiac output

• Vasodilation of the coronary and deep muscle arteries

• Vasoconstriction of blood vessels in the skin, abdominal viscera, and kidneys

• Increased blood coagulation and decreased clotting time

• Increased glycogenolysis, the conversion of stored sugar (glycogen) to glucose

• Increased release of glucose from the liver (raises blood glucose)

• Inhibited digestion

• Increased arterial blood pressure

Increased metabolic rate

• Increased brain activity

• Increased sweat gland activity

• Dilation of bronchioles in the lungs

• Increased respiration rate and depth

• Dilation of pupils

• Increased skeletal muscle contractility

• Breakdown of fatty tissue, raising blood fatty acid (FFA) levels, triglycerides, and/or cholesterol

B represents the intermediate pathway due to the delayed onset and longer duration of effects. A neuron originates in the spine and terminates in the adrenal medulla. When activated, it stimulates the adrenal medulla to release epinephrine (Epi) and norepinephrine (NE) into the circulation; the longer-acting nature of hormones serves to sustain the stress response. The combined effects of Epi and NE are an increase in blood pressure and cardiac output. The specific effects are:

• Increased heart rate, stroke volume, and cardiac output

• Vasodilation of the coronary arteries

• Increased glycogenolysis

• Increased glucose release from the liver

• Vasoconstriction of peripheral skin arterioles

• Vasoconstriction of superficial muscle arterioles

• Increased blood coagulation and decreased clotting time

The remaining pathways are long-term pathways involving the pituitary, a gland situated just under the hypothalamus. The pituitary is referred to as the "master" endocrine gland, as it controls the activity of other endocrine glands. The anterior pituitary releases trophic hormones (ACTH and TSH) into the bloodstream, which in turn stimulate other endocrine glands (i.e., adrenal cortex and thyroid) to release hormones (i.e., Cortisol, aldosterone, thyroxine) into the bloodstream. In turn, these hormones target and excite various tissues and organs (e.g., liver, kidneys, heart, and arterioles).

C represents the ACTH pathway. This is a long-term pathway in which ACTH (adrenocorticotrophic hormone) is released from the anterior pituitary and targets the adrenal cortex. The adrenal cortex responds by releasing glucocorticoids and mineralocorticoids. The chief glucocorticoid is Cortisol (Cor), which has numerous, potentially detrimental effects. Those related to cardiovascular disease include:

• Elevated insulin levels and abdominal fat storage

• Mobilization of fatty acids from fat cells

• Increased gluconeogenesis, the liver's formation of glucose from amino acids and other molecules

• Increased blood glucose

Cortisol also decreases the number and/or activity of white blood cells and plays a role in the atrophy of lymphatic structures including the thymus, thereby potentially compromising the immune system. It also acts with Epi to produce anti-inflammatory effects. The chief mineralocorticoid is aldosterone (Aid), which maintains blood sodium homeostasis via increased sodium retention, increased water retention by the kidneys, and increased blood and interstitial fluid volume. Aldosterone also has an inflammatory effect and increases cardiac output.

D represents the thyroxine (Thy) pathway, one of the most significant because of the duration of its effects. Thyroid stimulating hormone (TSH) is released from the anterior pituitary and targets the thyroid, which releases thyroxine. This hormone has numerous physiological effects, many of which are implicated in cardiovascular disease, including:

• Increased metabolic rate via an increase in general metabolism in almost all cells

• Increased (cellular) oxygen consumption

• Increased respiration rate and depth

• Increased heart rate and cardiac output

• Increased peripheral resistance

• In general, an increase in protein catabolism

• Increased internal body temperature

• Increased gastrointestinal motility, absorption, and secretion of digestive juices

• Increased cerebration (i.e., irritability, anxiety, and insomnia)

Regarding the vasopressin pathway, E, the anterior hypothalamus stimulates the posterior pituitary to release the neurotransmitter vasopressin, a potent vasoconstrictor. Its effects result in increased smooth muscle contraction (clamping of the arteries), increased renal permeability to water, water reabsorption, decreased perspiration, increased blood volume, and increased arterial blood pressure. There are several theories that suggest that transient increases in blood pressure may result in sustained hypertension, a form of cardiovascular disease and a primary risk factor for coronary artery disease.

The endothelial injury hypothesis has been proposed to explain the involvement of the various pathways in the development of coronary artery disease, the most prevalent cardiovascular disease. The theory posits that injury to the thin layer of endothelial cells of the arterial wall triggers the initiation of plaque formation. This injury may occur as the result of mechanical forces (i.e., blood pressure increases hemodynamic forces on arterial wall) or via chemical means (i.e., increased LDL-C, catecholamines, corticoids, etc.). Atherosclerosis is the process that entails endothelial injury, plaque formation, lesion development, and subsequent plaque buildup.

Figure C. 1 Stress, Anger, and Cardiovascular Disease: A Comprehensive Model

(by Melissa Hallmark Kerr)


TSH: Thyroid Stimulating Hormone

HDL-C: High Density Lipoprotein Cholesterol FFA: Free Fatty Acids CVD: Cardiovascular Disease

Neuroendocrine Effects:



Epi: Epinephrine

NE: Norepinephrine

Cor: Cortisol

Aid: Aldosterone

Thy: Thyroxine

MAP: Mean Arterial Pressure

ACTH: Adrenocorticotrophic Hormone

(blood pressure) LDL-C: Low Density Lipoprotein Cholesterol



Core Belief(s)









Liver Kidneys Heart Arterioles Other Organs


Liver Kidneys Heart Arterioles Other Organs t MAP

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