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Does Prolonged Stress Increase the Likelihood of a Stroke?

2687 words (11 pages) Essay in Medical

08/02/20 Medical Reference this

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3

Introduction

Appropriate physiological responses to stress are important for survival. The

hypothalamic-pituitary-adrenocortical (HPA) axis and the sympatho-adrenomedullary axis are

the primary systems that are responsible for the maintenance of homeostasis during stress, and

the adrenal gland is an essential organ that is common to both systems. For the HPA axis

(reviewed in (37)), hypophysiotropic neurons in the paraventricular nucleus of the hypothalamus

(PVN) secrete releasing hormones, such as corticotropin releasing hormone (CRH) and

vasopressin, into the portal circulation of the median eminence. These releasing hormones act on

the anterior pituitary to promote the secretion of adrenocorticotropic hormone (ACTH) into the

produce glucocorticoid hormones (e.g. corticosterone in rats and cortisol in humans). In

addition, ACTH can stimulate the outer adrenal cortex (i.e. the zona glomerulosa) to produce

hormones into the systemic circulation. Collectively, the glucocorticoid and catecholamine

hormones have complementary actions throughout the body, including energy mobilization and

maintenance of blood pressure (35).

While the stress responses described above are imperative for survival during acute

stress, frequent or prolonged activation can change the functional tone of these systems.

Previous work looking at the effects of chronic stress on the HPA axis has largely focused on

characterizing chronic stress-induced brain alterations, such as increased expression of CRH and

4

vasopressin in the PVN and decreased expression of glucocorticoid receptors in the hippocampus

and PVN (36, 47, 57, 67). This central focus has occurred in part because the observed brain

changes resemble those that are believed to occur in some types of stress-related psychiatric

disorders, such as depression and anxiety (6, 9, 22, 23, 39, 46). However, rats exposed to

despite normal plasma ACTH levels, suggesting that chronic stress also affects the peripheral

limb of the HPA axis (31, 49, 58, 59, 63, 84). Moreover, many patients with depression have

increased basal plasma cortisol and enlarged adrenals (4, 15, 24, 25, 64, 71, 72, 77).

Furthermore, increased glucocorticoid levels have been linked with the onset and severity of

depression (22, 32), suggesting that alterations in peripheral HPA axis structure and function

The purpose of the current study is to use a chronic variable stress (CVS) paradigm in

rats to characterize the effects of chronic stress on adrenal morphology and cortical function.

Early in vivo work using one or two doses of ACTH suggests that adrenal responses to ACTH

are increased following chronic stress (7, 8, 70); however, it is not known whether enhanced

responsiveness is due to increased sensitivity to ACTH (e.g. lower half-maximal dose, or ED50)

Also, it is not clear whether

adrenal enlargement following chronic stress is due to cellular hypertrophy (increased cell size)

and/or hyperplasia (increased number of cells), and whether these types of growth are restricted

The present work addresses the hypothesis that

adrenal responses to ACTH (both sensitivity and efficacy) are augmented after chronic stress,

and that this increased responsiveness is associated with cellular hypertrophy and hyperplasia in

the zona fasciculata.

3

Introduction

Appropriate physiological responses to stress are important for survival. The

hypothalamic-pituitary-adrenocortical (HPA) axis and the sympatho-adrenomedullary axis are

the primary systems that are responsible for the maintenance of homeostasis during stress, and

the adrenal gland is an essential organ that is common to both systems. For the HPA axis

(reviewed in (37)), hypophysiotropic neurons in the paraventricular nucleus of the hypothalamus

(PVN) secrete releasing hormones, such as corticotropin releasing hormone (CRH) and

vasopressin, into the portal circulation of the median eminence. These releasing hormones act on

the anterior pituitary to promote the secretion of adrenocorticotropic hormone (ACTH) into the

systemic circulation. ACTH acts on the inner adrenal cortex (i.e. the zona fasciculata) to

produce glucocorticoid hormones (e.g. corticosterone in rats and cortisol in humans). In

addition, ACTH can stimulate the outer adrenal cortex (i.e. the zona glomerulosa) to produce

aldosterone (30), in concert with the renin-angiotensin system. For the sympatho-

adrenomedullary system (reviewed in (35)), neural activation of the sympathetic nervous system

results in the “fight or flight” response, which includes activation of neurally-derived chromaffin

cells in the adrenal medulla. Chromaffin cells release catecholamines and neuropeptide

hormones into the systemic circulation. Collectively, the glucocorticoid and catecholamine

hormones have complementary actions throughout the body, including energy mobilization and

maintenance of blood pressure (35).

While the stress responses described above are imperative for survival during acute

stress, frequent or prolonged activation can change the functional tone of these systems.

Previous work looking at the effects of chronic stress on the HPA axis has largely focused on

characterizing chronic stress-induced brain alterations, such as increased expression of CRH and

4

vasopressin in the PVN and decreased expression of glucocorticoid receptors in the hippocampus

and PVN (36, 47, 57, 67). This central focus has occurred in part because the observed brain

changes resemble those that are believed to occur in some types of stress-related psychiatric

disorders, such as depression and anxiety (6, 9, 22, 23, 39, 46). However, rats exposed to

chronic stress often exhibit adrenal enlargement and increased basal plasma corticosterone

despite normal plasma ACTH levels, suggesting that chronic stress also affects the peripheral

limb of the HPA axis (31, 49, 58, 59, 63, 84). Moreover, many patients with depression have

increased basal plasma cortisol and enlarged adrenals (4, 15, 24, 25, 64, 71, 72, 77).

Furthermore, increased glucocorticoid levels have been linked with the onset and severity of

depression (22, 32), suggesting that alterations in peripheral HPA axis structure and function

may also be clinically relevant .

The purpose of the current study is to use a chronic variable stress (CVS) paradigm in

rats to characterize the effects of chronic stress on adrenal morphology and cortical function.

Early in vivo work using one or two doses of ACTH suggests that adrenal responses to ACTH

are increased following chronic stress (7, 8, 70); however, it is not known whether enhanced

responsiveness is due to increased sensitivity to ACTH (e.g. lower half-maximal dose, or ED50)

and/or elevated maximal output (e.g. higher efficacy, or Bmax). Also, it is not clear whether

adrenal enlargement following chronic stress is due to cellular hypertrophy (increased cell size)

and/or hyperplasia (increased number of cells), and whether these types of growth are restricted

to specific subregions of the adrenal gland. The present work addresses the hypothesis that

adrenal responses to ACTH (both sensitivity and efficacy) are augmented after chronic stress,

and that this increased responsiveness is associated with cellular hypertrophy and hyperplasia in

the zona fasciculata.

propriate physiological responses to stress are important for survival. The

hypothalamic-pituitary-adrenocortical (HPA) axis and the sympatho-adrenomedullary axis are

the primary systems that are responsible for the maintenance of homeostasis during stress, and

the adrenal gland is an essential organ that is common to both systems. For the HPA axis

(reviewed in (37)), hypophysiotropic neurons in the paraventricular nucleus of the hypothalamus

(PVN) secrete releasing hormones, such as corticotropin releasing hormone (CRH) and

vasopressin, into the portal circulation of the median eminence. These releasing hormones act on

the anterior pituitary to promote the secretion of adrenocorticotropic hormone (ACTH) into the

systemic circulation. ACTH acts on the inner adrenal cortex (i.e. the zona fasciculata) to

produce glucocorticoid hormones (e.g. corticosterone in rats and cortisol in humans). In

addition, ACTH can stimulate the outer adrenal cortex (i.e. the zona glomerulosa) to produce

aldosterone (30), in concert with the renin-angiotensin system. For the sympatho-

adrenomedullary system (reviewed in (35)), neural activation of the sympathetic nervous system

results in the “fight or flight” response, which includes activation of neurally-derived chromaffin

cells in the adrenal medulla. Chromaffin cells release catecholamines and neuropeptide

hormones into the systemic circulation. Collectively, the glucocorticoid and catecholamine

hormones have complementary actions throughout the body, including energy mobilization and

maintenance of blood pressure (35).

While the stress responses described above are imperative for survival during acute

stress, frequent or prolonged activation can change the functional tone of these systems.

Previous work looking at the effects of chronic stress on the HPA axis has largely focused on

characterizing chronic stress-induced brain alterations, such as increased expression of CRH and

4

vasopressin in the PVN and decreased expression of glucocorticoid receptors in the hippocampus

and PVN (36, 47, 57, 67). This central focus has occurred in part because the observed brain

changes resemble those that are believed to occur in some types of stress-related psychiatric

disorders, such as depression and anxiety (6, 9, 22, 23, 39, 46). However, rats exposed to

chronic stress often exhibit adrenal enlargement and increased basal plasma corticosterone

despite normal plasma ACTH levels, suggesting that chronic stress also affects the peripheral

limb of the HPA axis (31, 49, 58, 59, 63, 84). Moreover, many patients with depression have

increased basal plasma cortisol and enlarged adrenals (4, 15, 24, 25, 64, 71, 72, 77).

Furthermore, increased glucocorticoid levels have been linked with the onset and severity of

depression (22, 32), suggesting that alterations in peripheral HPA axis structure and function

may also be clinically relevant .

The purpose of the current study is to use a chronic variable stress (CVS) paradigm in

rats to characterize the effects of chronic stress on adrenal morphology and cortical function.

Early in vivo work using one or two doses of ACTH suggests that adrenal responses to ACTH

are increased following chronic stress (7, 8, 70); however, it is not known whether enhanced

responsiveness is due to increased sensitivity to ACTH (e.g. lower half-maximal dose, or ED50)

and/or elevated maximal output (e.g. higher efficacy, or Bmax). Also, it is not clear whether

adrenal enlargement following chronic stress is due to cellular hypertrophy (increased cell size)

and/or hyperplasia (increased number of cells), and whether these types of growth are restricted

to specific subregions of the adrenal gland. The present work addresses the hypothesis that

adrenal responses to ACTH (both sensitivity and efficacy) are augmented after chronic stress,

and that this increased responsiveness is associated with cellular hypertrophy and hyperplasia in

the zona fasciculata.

Research Project: Negative Group

Introduction:

At this very moment, regulation of our cardiovascular system and cerebral blood flow is working to deliver nutrients, oxygen and chemical exchanges to the body. The brain is the alpha control center. It is the key organ to coping with any recovery process within the body because it determines what is threating or stressful to the individual. Any slight deviation would be accessed and quickly decided by the brain to bring the body’s environment back to homeostasis. So how does the brain affect the cardiovascular system when it comes to balancing blood flow? To begin, we must look at the endothelium of the heart which is a thin membrane that lies inside the heart and blood vessels that function as a regulator of blood flow. Cardiac output and blood flow rely heavily on vascular relaxation and contraction. During times of normal stress epinephrine and norepinephrine are released into the blood stream by way of the medulla oblongata and ANS, specifically the sympathetic nervous system which increases heart rate, blood pressure, and respiratory rate. To counter this response, the hypothalamus region of our brain activates hormones such as corticotropin, a hormone involved in stress response into the blood circulation to achieve stabilization. (via www.ncbi.nlm.nih.gov ) However, if there were to be a prolonged stimulus of stress the normal response of these regions would be altered and the negative feedback mechanism would be disrupted. This would include heart rate, vascular tone and inflammation alterations within the blood vessel and heart. As a group we believe that focusing on the principal effects that manifest from negative terminations can be correlated to brain behavior and stress. It then bears the question; does prolonged chronic stress (psychological: anxiety, fear, depression) increase the likelihood of a stroke?

     The two studies read for our research were, “Stress Worsens Endothelial function and Ischemic stroke via Glucocorticoids” (via www.ahajournals.org), and “Impact of psychological health on peripheral endothelial function and the HPA-axis activity in healthy adolescents” (via www.atherosclerosis-journal.com) These two articles coincided and allowed us to focus on one hypothesis.

The first study read, used mice models in their experiment and exposed them to long periods of stress, which included restraint stress, tail suspension, and exposure to rat. Each of these situations caused an upturn in heart rate and mildly affected blood pressure. The results of this experiment confirm that “certain psychological factors with continued exposure increases heart rate when induced by stress” (via www.ahajournals.org). It further explains that “exposure to stress has been considered as an independent risk factor for stroke and dysregulation of the hypothalamic-pituitary –adrenal axis and proposed that it can negatively affect stroke outcome” (via www.ahajournals.org). For instance, during the data collection low endothelium function was observed and found to correlate with a decrease of the enzyme eNOS, which produces nitric oxide. As per the Journal of Cell Science, “endothelium-derived nitric oxide (NO) is a critical regulator of cardiovascular homeostasis” (via www.jcs.biologists.org). This particular enzyme is vital for a healthy cardiovascular system. It is clear then, that definite effects of negative stress on the brain can manifest physiological distress and cause damage to the cardiovascular system.

The second study focused on psychosocial stress in adolescent boys and girls, and the effects it may have on the cardiovascular system. The study followed these adolescents for a period of three years and collected data through various methods (details to follow) to determine the degree of stress that it may have had on endothelial function. Specifically, this reading went on to state, “that a longitudinal study provides evidence supporting the contention that psychological health during adolescence plays an important role in peripheral endothelial function and the HPA axis activity” (via www.atherosclerosis-journal.com). Similar to the first reading, this study illustrates that a high level of stress can cause adverse changes in the cardiovascular system. With this in mind, we can delve deeper into the physiological disorders that occur with prolonged periods of chronic stress like increased heart rate and endothelial dysfunction. Therefore, our emphasis relies on the stress conditions of the brain and the effect it has on the cardiovascular system.

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