ACTH Secreted By: Unlock the Mystery!

Adrenocorticotropic hormone, more commonly known as ACTH, is a vital peptide hormone that plays a central role in the body’s endocrine system. Its primary function is to stimulate the adrenal glands, specifically the adrenal cortex, to produce and release cortisol, a crucial hormone involved in stress response, metabolism, and immune function. Understanding the intricacies of ACTH secretion is not merely an academic exercise; it’s fundamental to comprehending overall health and effectively diagnosing a range of related diseases.

ACTH: The Conductor of the Adrenal Orchestra

ACTH, produced by the anterior pituitary gland, acts as a messenger, traveling through the bloodstream to reach its target: the adrenal glands.

Upon arrival, ACTH binds to receptors on cells within the adrenal cortex.

This interaction triggers a cascade of intracellular events.

These events ultimately lead to the synthesis and release of cortisol.

Cortisol is essential for regulating blood sugar levels, modulating the immune response, and helping the body cope with stress.

The Significance of Understanding ACTH Secretion

The precise regulation of ACTH secretion is paramount for maintaining hormonal balance and overall well-being. Deviations from normal ACTH levels, whether too high or too low, can indicate underlying medical conditions that require careful evaluation and treatment.

Disruptions in ACTH secretion can manifest in various ways, leading to a spectrum of clinical presentations.

For example, excessive ACTH secretion can lead to Cushing’s disease, characterized by weight gain, high blood pressure, and muscle weakness.

Conversely, insufficient ACTH secretion can result in adrenal insufficiency, leading to fatigue, low blood pressure, and potentially life-threatening adrenal crises.

Therefore, understanding the factors that influence ACTH secretion, as well as the mechanisms that regulate its production and release, is crucial for clinicians. It empowers them to accurately diagnose and manage a wide range of endocrine disorders, improving patient outcomes and quality of life.

ACTH’s crucial role in regulating the body’s stress response, metabolism, and immune function is undeniable. But where does this essential hormone originate? The answer lies within a small, yet powerful gland nestled deep within the brain.

The Master Gland: The Anterior Pituitary’s Role in ACTH Production

The anterior pituitary gland stands as the undisputed orchestrator of ACTH production. This tiny endocrine gland, often referred to as the "master gland," plays a critical role in regulating various bodily functions through the secretion of different hormones, including ACTH.

The Anterior Pituitary: Main Source of ACTH

The anterior pituitary gland is the primary source of ACTH in the body. It’s the central command center responsible for synthesizing, storing, and releasing ACTH into the bloodstream.

Think of it as the main factory where ACTH is meticulously crafted and prepared for its vital mission. Without the anterior pituitary, the body would be unable to effectively respond to stress, regulate cortisol levels, and maintain overall hormonal balance.

Location and Structure

Nestled at the base of the brain, just below the hypothalamus, the anterior pituitary gland occupies a protected space within the sella turcica, a bony structure of the sphenoid bone. This strategic location allows it to communicate closely with the hypothalamus, which exerts significant control over its functions.

Structurally, the anterior pituitary is composed of various types of endocrine cells. These cells are responsible for producing different hormones.

Among these cells, the corticotrophs are the dedicated specialists responsible for synthesizing and secreting ACTH. The intricate network of blood vessels within the anterior pituitary ensures that hormones, including ACTH, can be quickly released into the circulation to reach their target organs.

The intricate network of endocrine cells within the anterior pituitary orchestrates a symphony of hormonal secretions, and among these cells, a specialized group takes center stage in the production of ACTH: the corticotrophs.

Corticotrophs: The Specialized ACTH Factories

These dedicated cells are the primary producers of ACTH within the anterior pituitary gland, acting as miniature factories that synthesize, process, store, and secrete this vital hormone.

Understanding the inner workings of corticotrophs and the mechanisms that govern their ACTH production is crucial for unraveling the complexities of the stress response and related hormonal imbalances.

Identifying Corticotrophs: Location and Characteristics

Corticotrophs are found throughout the anterior pituitary, interspersed among other endocrine cell types.

These cells, like other hormone-producing cells, possess unique characteristics that enable them to fulfill their specialized function.

They are typically identified by their distinct morphology and the presence of specific markers, such as the ACTH protein itself, which can be detected through immunohistochemical staining.

Corticotrophs exhibit features characteristic of active protein-synthesizing cells, including a well-developed endoplasmic reticulum and Golgi apparatus.

These organelles are essential for the synthesis, processing, and packaging of ACTH into secretory granules.

The ACTH Production Line: From Gene to Hormone

The production of ACTH within corticotrophs is a complex process involving several key steps:

1. Gene Transcription: The process begins with the transcription of the POMC (Pro-opiomelanocortin) gene into messenger RNA (mRNA).

2. mRNA Translation: The mRNA molecule then travels to the ribosomes, where it directs the synthesis of a large precursor protein called POMC.

3. POMC Processing: POMC is subsequently cleaved by specific enzymes to generate various peptide hormones, including ACTH, melanocyte-stimulating hormone (MSH), and endorphins.

4. Packaging and Storage: The newly synthesized ACTH is then packaged into secretory granules, where it is stored until a signal triggers its release.

Regulation of ACTH Production: A Delicate Balance

ACTH production within corticotrophs is tightly regulated by a variety of factors, ensuring that the body’s needs are met while preventing excessive or insufficient hormone secretion.

CRH: The Primary Stimulator

Corticotropin-Releasing Hormone (CRH), produced by the hypothalamus, is the primary stimulator of ACTH release from corticotrophs.

CRH binds to specific receptors on the surface of corticotrophs, triggering a cascade of intracellular signaling events that ultimately lead to increased ACTH synthesis and secretion.

Glucocorticoid Feedback: Maintaining Equilibrium

Glucocorticoids, such as cortisol, exert a negative feedback effect on ACTH production.

Elevated cortisol levels inhibit the release of both CRH from the hypothalamus and ACTH from the anterior pituitary, preventing excessive stimulation of the adrenal glands.

Other Regulatory Factors

Other factors that can influence ACTH production include:

• Arginine vasopressin (AVP) which can potentiate the effects of CRH.

• Cytokines and inflammatory mediators, which can stimulate ACTH release during stress or illness.

• Circadian rhythms, resulting in diurnal variations in ACTH levels.

Dysregulation of Corticotroph Function: Clinical Implications

Disruptions in the normal function of corticotrophs can lead to a variety of clinical disorders:

• Cushing’s Disease: Pituitary adenomas, or tumors of the pituitary gland, may arise from the corticotroph cells. This leads to excessive ACTH production and subsequently hypercortisolism.

• Nelson’s Syndrome: Removal of the adrenal glands without addressing an underlying corticotroph adenoma can result in rapid growth of the tumor and extremely high ACTH levels.

• ACTH Deficiency: Damage or dysfunction of the anterior pituitary can lead to ACTH deficiency, resulting in adrenal insufficiency and a decreased ability to respond to stress.

Understanding the intricate workings of corticotrophs is paramount in elucidating the pathophysiology of these disorders and developing targeted therapies to restore hormonal balance.

The corticotrophs, as we’ve seen, are the dedicated cells responsible for ACTH production. But their activity isn’t autonomous. The anterior pituitary, while a crucial hub, is itself under the influence of a higher command center, a region of the brain that orchestrates a wide array of bodily functions: the hypothalamus. This connection, mediated by a vital hormone, forms the crux of a critical regulatory pathway.

The Hypothalamic Connection: CRH’s Stimulatory Power

The hypothalamus and the anterior pituitary gland are intricately linked, forming a vital axis that governs numerous hormonal functions within the body. This connection isn’t a direct neural pathway, but rather a specialized vascular network through which the hypothalamus communicates using releasing and inhibiting hormones.

The Hypothalamus-Pituitary Portal System

The hypothalamus, a small but mighty region located at the base of the brain, acts as a central control center, integrating various signals from the body and the environment. It plays a key role in regulating body temperature, hunger, thirst, sleep-wake cycles, and, importantly, hormonal balance.

The anterior pituitary, situated just below the hypothalamus, is a major endocrine gland responsible for producing and releasing several crucial hormones, including ACTH. However, the anterior pituitary doesn’t operate independently; its hormonal output is tightly regulated by the hypothalamus.

The connection between these two structures is unique, utilizing a specialized circulatory system known as the hypothalamic-pituitary portal system.

This system allows for the direct and efficient transport of hormones from the hypothalamus to the anterior pituitary, ensuring that these regulatory signals reach their target cells with minimal dilution or degradation.

Instead of directly innervating the anterior pituitary, hypothalamic neurons release hormones into the portal system’s capillaries.

These capillaries then drain into portal veins that travel down the pituitary stalk and into the anterior pituitary gland.

Within the anterior pituitary, these portal veins branch into a second capillary network, delivering the hypothalamic hormones directly to the endocrine cells, including the corticotrophs.

CRH: The Primary Stimulator of ACTH Release

Corticotropin-Releasing Hormone (CRH) stands as the primary stimulator of ACTH release from the anterior pituitary.

Produced by specialized neurons within the hypothalamus, CRH acts as a crucial messenger, initiating the cascade of events that ultimately lead to cortisol production by the adrenal glands.

When the hypothalamus senses a need for increased cortisol levels – often in response to stress, low blood sugar, or other physiological challenges – it releases CRH into the hypothalamic-pituitary portal system.

Upon reaching the anterior pituitary, CRH binds to specific receptors on the surface of corticotroph cells.

This binding triggers a series of intracellular signaling events within the corticotrophs, ultimately leading to the synthesis and secretion of ACTH.

The amount of ACTH released is directly proportional to the amount of CRH stimulation, ensuring a finely tuned response to the body’s needs.

CRH’s Journey: From Hypothalamus to Anterior Pituitary

The journey of CRH from the hypothalamus to the anterior pituitary is a precisely orchestrated process.

CRH-producing neurons, located in the paraventricular nucleus (PVN) of the hypothalamus, synthesize and package CRH into secretory vesicles.

Upon appropriate stimulation, these neurons release CRH into the interstitial space surrounding the capillaries of the hypothalamic-pituitary portal system.

Due to the proximity of the PVN to the portal system, CRH can rapidly diffuse into the capillaries and be transported to the anterior pituitary.

This efficient delivery mechanism ensures that CRH reaches the corticotrophs quickly and effectively, allowing for a rapid ACTH response when needed.

The entire process, from CRH release in the hypothalamus to ACTH secretion in the anterior pituitary, can occur within minutes, highlighting the speed and efficiency of this crucial regulatory pathway.

Destination Adrenal Glands: ACTH’s Target Organs

Having traversed the intricate network connecting the hypothalamus and pituitary, ACTH now embarks on the final leg of its journey. Its destination: the adrenal glands. It is here, within these vital organs, that ACTH exerts its primary influence, triggering a cascade of hormonal events critical for maintaining homeostasis and responding to stress.

The Adrenal Glands: Anatomy and Location

The adrenal glands, also known as suprarenal glands, are paired endocrine glands situated atop each kidney.

Each gland is composed of two distinct regions: the outer cortex and the inner medulla.

The adrenal cortex, which constitutes the majority of the gland, is responsible for producing a variety of steroid hormones, including cortisol, aldosterone, and androgens.

It is the adrenal cortex’s zona fasciculata that is the primary site of cortisol synthesis.

ACTH’s Mechanism of Action on Adrenal Cells

ACTH’s arrival at the adrenal glands marks the initiation of a crucial signaling pathway.

ACTH binds to specific receptors on the surface of adrenocortical cells, primarily within the zona fasciculata.

This binding activates a G protein-coupled receptor, initiating a series of intracellular events.

The G protein stimulates adenylate cyclase, an enzyme that converts ATP into cyclic AMP (cAMP), a second messenger molecule.

The Role of cAMP in Cortisol Synthesis

cAMP acts as a key regulator of cortisol synthesis.

It activates protein kinase A (PKA), which then phosphorylates and activates various enzymes involved in the steroidogenic pathway.

This pathway is a complex series of enzymatic reactions that convert cholesterol into cortisol.

A crucial step involves the transport of cholesterol into the mitochondria, facilitated by the steroidogenic acute regulatory protein (StAR).

StAR is considered the rate-limiting step in cortisol production, and its expression is highly sensitive to ACTH stimulation.

Cortisol Production and Release

Under ACTH stimulation, the adrenal cortex ramps up cortisol production.

Synthesized cortisol is then released into the bloodstream, where it travels to target tissues throughout the body.

The amount of cortisol released is directly proportional to the level of ACTH stimulation, ensuring a rapid and appropriate response to changing physiological demands.

This intricate mechanism highlights the crucial role of ACTH in regulating adrenal gland function and maintaining cortisol levels within a tightly controlled range.

Cortisol: The End Product and Its Multifaceted Roles

Having explored the intricate pathways leading to cortisol synthesis within the adrenal cortex, it’s essential to understand the far-reaching effects of this hormone throughout the body. Cortisol, often dubbed the "stress hormone," plays a pivotal role in numerous physiological processes. These functions extend far beyond simply managing stress.

Diverse Functions of Cortisol

Cortisol exerts its influence on virtually every organ system. Its actions are diverse and essential for maintaining homeostasis. From regulating blood sugar levels to modulating immune responses, cortisol’s presence is vital for proper bodily function.

• Metabolic Regulation: Cortisol is deeply involved in glucose metabolism. It promotes gluconeogenesis (the production of glucose from non-carbohydrate sources) in the liver. This action helps to raise blood sugar levels, providing the body with energy during times of stress or fasting.

  It also influences the metabolism of proteins and fats. Cortisol promotes the breakdown of proteins into amino acids, which can then be used for gluconeogenesis or tissue repair. In addition, it facilitates the mobilization of fatty acids from adipose tissue, providing an alternative energy source.

• Immune Modulation: Cortisol has well-established anti-inflammatory and immunosuppressive effects. It suppresses the production of pro-inflammatory cytokines, reducing inflammation throughout the body. This can be beneficial in controlling autoimmune disorders or allergic reactions.

  However, chronic elevation of cortisol can impair immune function. This can increase susceptibility to infections and delay wound healing. The delicate balance between cortisol’s beneficial and detrimental effects on the immune system is crucial.

• Cardiovascular Function: Cortisol influences blood pressure and cardiovascular responsiveness. It enhances the effects of catecholamines (such as adrenaline) on blood vessels, leading to vasoconstriction and increased blood pressure. This is important for maintaining adequate blood flow during stress.

  Prolonged exposure to high levels of cortisol can contribute to hypertension and increase the risk of cardiovascular disease. Maintaining healthy cortisol levels is essential for cardiovascular health.

• Bone Metabolism: Cortisol affects bone formation and resorption. Chronic exposure to elevated cortisol levels can inhibit bone formation and increase bone resorption, leading to osteoporosis. This is a significant concern for individuals with Cushing’s syndrome or those on long-term glucocorticoid therapy.

• Central Nervous System: Cortisol has effects on the brain and central nervous system. It can influence mood, behavior, and cognitive function. Dysregulation of cortisol levels has been implicated in mood disorders such as depression and anxiety.

Cortisol’s Role in Stress Response

Cortisol’s reputation as the "stress hormone" is well-deserved. It is a key player in the body’s response to physical, emotional, or psychological stress. When faced with a stressor, the hypothalamus triggers the release of CRH. This initiates the cascade of hormonal events culminating in cortisol secretion.

Cortisol’s effects during stress are designed to help the body cope with the challenge. It provides energy by raising blood sugar levels. It suppresses inflammation to minimize tissue damage. It enhances cardiovascular function to ensure adequate oxygen delivery to tissues.

However, the chronic activation of the stress response system and prolonged exposure to elevated cortisol levels can have detrimental effects on health.

Impact on Metabolism

Cortisol’s influence on metabolism is profound. Its effects on glucose, protein, and fat metabolism can have significant implications for energy balance and body composition.

• Glucose Metabolism: Cortisol’s promotion of gluconeogenesis can lead to elevated blood sugar levels. This can contribute to insulin resistance and an increased risk of type 2 diabetes, especially in individuals who are already predisposed to these conditions.

• Protein Metabolism: The breakdown of proteins induced by cortisol can lead to muscle wasting and weakness. This is particularly concerning in individuals who are chronically stressed or have conditions associated with elevated cortisol levels.

• Fat Metabolism: Cortisol’s facilitation of fat mobilization can lead to increased levels of circulating fatty acids. These can be stored in visceral fat depots, increasing the risk of metabolic disorders such as heart disease and non-alcoholic fatty liver disease.

Impact on Immune Function

While cortisol has anti-inflammatory effects, chronic exposure to elevated levels can impair immune function. This can increase susceptibility to infections and delay wound healing.

Cortisol suppresses the activity of various immune cells, including lymphocytes and macrophages. It also inhibits the production of antibodies, which are essential for fighting off infections.

The delicate balance between cortisol’s beneficial and detrimental effects on the immune system is crucial for maintaining optimal health.

Impact on Overall Health

The multifaceted roles of cortisol highlight its importance in maintaining overall health and well-being. However, imbalances in cortisol levels, whether too high or too low, can have significant consequences.

Conditions associated with excessive cortisol production, such as Cushing’s syndrome, can lead to a wide range of symptoms, including weight gain, muscle weakness, skin changes, and increased susceptibility to infections.

Conditions associated with insufficient cortisol production, such as Addison’s disease, can lead to fatigue, weakness, weight loss, and low blood pressure.

Understanding the diverse functions of cortisol and the factors that influence its secretion is essential for maintaining optimal health and preventing disease.

Stress Response: The Cascade of Hormonal Activity

Cortisol’s wide-ranging effects underscore its importance, but understanding how its release is triggered is equally critical. The body’s response to stress provides a prime example of the intricate interplay between the nervous and endocrine systems, orchestrated to maintain equilibrium. This section delves into the mechanisms by which stress acts as a potent stimulus for ACTH secretion.

The Hypothalamic-Pituitary-Adrenal (HPA) Axis

The body’s stress response is largely governed by the hypothalamic-pituitary-adrenal (HPA) axis. This axis represents a complex feedback loop involving the hypothalamus, the anterior pituitary gland, and the adrenal glands.

When the brain perceives a threat, whether physical or psychological, a cascade of events is set in motion. The hypothalamus, acting as the control center, initiates the hormonal response.

CRH: The First Responder

The hypothalamus responds to stress by releasing corticotropin-releasing hormone (CRH). CRH is secreted into the hypophyseal portal system, a specialized network of blood vessels that directly connects the hypothalamus to the anterior pituitary gland.

Upon reaching the anterior pituitary, CRH binds to specific receptors on corticotroph cells. This binding stimulates the synthesis and release of ACTH into the systemic circulation.

ACTH’s Journey to the Adrenal Glands

ACTH then travels through the bloodstream to its target organs: the adrenal glands. Upon arrival, ACTH binds to receptors on the cells of the adrenal cortex, primarily the zona fasciculata.

This binding triggers a series of intracellular events that ultimately lead to increased production and secretion of cortisol. The adrenal glands, stimulated by ACTH, release cortisol into the bloodstream, where it can exert its effects on various target tissues throughout the body.

Physiological Changes During Stress

The increased levels of cortisol during stress prepare the body for a "fight-or-flight" response. Glucose production is enhanced, providing immediate energy.

The cardiovascular system is stimulated, increasing heart rate and blood pressure to deliver oxygen and nutrients to muscles.

The immune system is modulated, although the long-term effects of chronic stress can be immunosuppressive.

This coordinated hormonal response is essential for adapting to acute stressors. However, chronic activation of the HPA axis can have detrimental effects on health, highlighting the importance of managing stress effectively.

Negative Feedback: Maintaining Hormonal Harmony

The intricate dance of hormones within the body requires precise orchestration to maintain equilibrium.

Following the cascade of events within the HPA axis, a critical regulatory mechanism ensures that cortisol levels don’t spiral out of control. This vital mechanism is known as negative feedback, a process that acts as the body’s own built-in thermostat for hormonal balance.

The Essence of Negative Feedback

Negative feedback is a fundamental biological process where the end product of a pathway inhibits its own production.

Think of it like a thermostat in your home: when the temperature reaches the set point, the heating system shuts off.

Similarly, in the HPA axis, cortisol acts as the "thermostat," signaling the hypothalamus and pituitary gland to reduce their activity once cortisol levels reach a sufficient level.

This prevents excessive hormone production and maintains homeostasis.

Cortisol’s Inhibitory Role: A Multi-pronged Approach

Cortisol exerts its inhibitory effects at multiple points within the HPA axis.

Primarily, it targets the hypothalamus and the anterior pituitary gland.

At the hypothalamus, cortisol inhibits the release of CRH (corticotropin-releasing hormone). By reducing CRH secretion, the stimulus for ACTH release from the pituitary gland is diminished.

Simultaneously, cortisol acts directly on the anterior pituitary to suppress the synthesis and release of ACTH. This dual action ensures a robust dampening of the stress response.

Molecular Mechanisms of Inhibition

The inhibitory effects of cortisol are mediated through glucocorticoid receptors (GRs), which are present in both the hypothalamus and the anterior pituitary gland.

When cortisol binds to these receptors, it triggers a cascade of intracellular events that ultimately lead to decreased gene expression of CRH and ACTH.

Specifically, the activated GR complex can bind to specific DNA sequences, altering the transcription of genes involved in the synthesis of these hormones.

This intricate molecular mechanism allows for fine-tuned control over the HPA axis.

Clinical Significance of Negative Feedback

The integrity of the negative feedback loop is crucial for maintaining hormonal balance and overall health.

Dysregulation of this feedback mechanism can lead to various clinical disorders.

For instance, in Cushing’s syndrome, excessive cortisol production, often due to an ACTH-secreting pituitary tumor, overrides the normal negative feedback control.

This results in chronically elevated cortisol levels and a range of associated symptoms.

Conversely, impaired negative feedback can contribute to conditions like adrenal insufficiency, where the adrenal glands don’t produce enough cortisol, leading to an overstimulation of the HPA axis in an attempt to compensate.

Feedback Resistance and Stress

Chronic stress can alter the sensitivity of the negative feedback loop, leading to what is sometimes referred to as glucocorticoid resistance.

In this state, the hypothalamus and pituitary become less responsive to the inhibitory effects of cortisol, resulting in a higher baseline level of HPA axis activity.

This can contribute to a range of stress-related disorders, highlighting the importance of managing stress to maintain a healthy hormonal balance.

When Things Go Wrong: Clinical Implications of ACTH Imbalance

The exquisite balance maintained by the HPA axis is vital for health. But what happens when this finely tuned system goes awry? The consequences of ACTH imbalances can manifest in a range of clinical disorders, highlighting the critical role of proper ACTH regulation.

Cushing’s Disease: The Perils of ACTH Excess

One of the most well-known conditions associated with excessive ACTH is Cushing’s disease. This disorder typically arises from a benign tumor (adenoma) within the anterior pituitary gland.

These tumors, often microscopic, relentlessly secrete ACTH. This, in turn, drives the adrenal glands to overproduce cortisol.

The sustained elevation of cortisol levels leads to a constellation of symptoms. These can include weight gain (particularly in the face and trunk), high blood pressure, muscle weakness, skin changes (like easy bruising and purple striae), and impaired glucose metabolism, potentially leading to diabetes.

The Role of Pituitary Tumors in ACTH Secretion

Pituitary tumors are the predominant cause of Cushing’s disease. These adenomas disrupt the normal regulatory mechanisms that govern ACTH production.

Unlike healthy corticotrophs, tumor cells are often unresponsive to the negative feedback signals from cortisol. This leads to autonomous and excessive ACTH secretion.

The size of the tumor doesn’t always correlate with the severity of the disease. Even small microadenomas can secrete enough ACTH to cause significant cortisol excess.

Ectopic ACTH Syndrome: A Less Common Culprit

While pituitary tumors are the most common cause, ectopic ACTH syndrome represents another, albeit less frequent, cause of ACTH-dependent Cushing’s syndrome. In this condition, non-pituitary tumors, such as small cell lung cancer or carcinoid tumors, secrete ACTH.

These tumors operate outside the normal HPA axis control mechanisms. This leads to an often rapid and severe form of Cushing’s syndrome.

Identifying the source of ectopic ACTH production can be challenging but is crucial for effective treatment.

Pro-opiomelanocortin (POMC): The Precursor Molecule

It’s important to remember that ACTH isn’t synthesized in isolation. It’s derived from a larger precursor molecule called pro-opiomelanocortin (POMC).

POMC undergoes processing by enzymes to yield not only ACTH but also other peptide hormones. These include melanocyte-stimulating hormone (MSH) and beta-endorphin.

Therefore, conditions affecting POMC production or processing can impact ACTH levels. They can also influence the levels of these related hormones.

In Cushing’s disease, both ACTH and other POMC-derived peptides may be elevated. This leads to additional clinical manifestations, such as skin pigmentation changes due to increased MSH.

Understanding the role of POMC provides a more complete picture of the complex hormonal changes associated with ACTH-related disorders.

So, that’s the lowdown on ACTH! Hope this helped clear things up about when acth is secreted by your body. Keep learning, and stay healthy!