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Related Concept Videos

Cushing Syndrome II: Pathophysiology01:19

Cushing Syndrome II: Pathophysiology

Cortisol production is normally governed by the hypothalamic–pituitary–adrenal (HPA) axis, which maintains hormonal balance through tightly regulated feedback mechanisms. Disruption of this regulatory system is central to the development of Cushing syndrome, whether the excess cortisol originates from external medications or internal pathology. Persistent cortisol elevation alters metabolism, immune function, and endocrine signaling, producing the characteristic clinical features of the...
Hormones of the Adrenal Glands01:31

Hormones of the Adrenal Glands

Adrenal hormones play a pivotal role in maintaining the body's electrolyte balance and orchestrating responses to stress, showcasing the intricate functions of the adrenal cortex and medulla.
The adrenal cortex, a powerhouse of hormone synthesis, generates over two dozen corticosteroid hormones. The zona glomerulosa produces mineralocorticoids, exemplified by aldosterone, influencing the electrolyte composition of body fluids. The synthesis of glucocorticoids such as cortisol and corticosterone...
Hypothalamic-Pituitary Axis01:37

Hypothalamic-Pituitary Axis

The response to stress—be it physical or psychological, acute or chronic—involves activation of the Hypothalamic-Pituitary-Adrenal (HPA) axis. The HPA axis is part of the neuroendocrine system because it involves both neuronal and hormonal communication. Its function is to regulate homeostatic systems—metabolic, cardiovascular, and immune—providing the necessary means to respond to a stressor.
Hypertension II: Pathophysiology01:29

Hypertension II: Pathophysiology

Hypertension is a chronic condition in which the blood's force against artery walls is excessively high, posing risks such as heart disease. The condition's underlying mechanisms involve complex interactions among the cardiovascular, kidney, and autonomic nervous systems.Renin-Angiotensin-Aldosterone System (RAAS): This system significantly influences blood pressure regulation. When blood pressure decreases, the kidneys secrete renin. This enzyme transforms angiotensinogen, a plasma protein,...
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

β1-receptors are primarily located in the heart and kidneys. In cardiac myocytes, these receptors interact with neurotransmitters released by the sympathetic nervous system during heightened activity or danger. As a result, β1-receptors get activated, initiating a series of biochemical processes. Excessive activation of beta receptors due to chronic stress can abnormally increase heart rate and contractility, resulting in high blood pressure or hypertension. To counteract this, β1-blockers...
Cushing Syndrome I: Introduction01:26

Cushing Syndrome I: Introduction

Cushing syndrome refers to the collection of clinical manifestations that arise when tissues are exposed to excessive amounts of cortisol or cortisol-like medications over an extended period. Cortisol, a glucocorticoid produced by the adrenal cortex, regulates metabolism, immune responses, and the body’s adaptation to stress. When its concentration remains chronically elevated, these physiological pathways become dysregulated, resulting in the characteristic features of the syndrome.Exogenous...

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Related Experiment Video

Updated: Jul 20, 2026

Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions
04:33

Primary Culture of Rat Adrenocortical Cells and Assays of Steroidogenic Functions

Published on: March 12, 2019

Cortisol metabolism in hypertension.

Fabian Hammer1, Paul M Stewart

  • 1Division of Medical Sciences, University of Birmingham, Institute of Biomedical Research, Birmingham B15 2TT, UK.

Best Practice & Research. Clinical Endocrinology & Metabolism
|September 19, 2006
PubMed
Summary

Corticosteroids significantly impact blood pressure. The enzymes 11beta-hydroxysteroid dehydrogenases (11beta-HSDs) regulate glucocorticoid action, influencing conditions like hypertension and hypotension.

Area of Science:

  • Endocrinology
  • Cardiovascular Physiology
  • Genetics

Background:

  • Corticosteroids are crucial for blood pressure regulation, with deficiencies (Addison's disease) causing hypotension and excesses (Cushing's syndrome) leading to hypertension.
  • 11beta-hydroxysteroid dehydrogenases (11beta-HSDs) modulate glucocorticoid activity at a pre-receptor level.
  • 11beta-HSD1 activates cortisone to cortisol, enhancing glucocorticoid receptor (GR) action, while 11beta-HSD2 inactivates cortisol to cortisone, protecting the mineralocorticoid receptor (MR) from cortisol in aldosterone target tissues.

Purpose of the Study:

  • To explore the role of corticosteroids and 11beta-hydroxysteroid dehydrogenases (11beta-HSDs) in blood pressure regulation.
  • To investigate the mechanisms by which 11beta-HSDs influence hypertension and related disorders.
  • To examine the impact of genetic variations and environmental factors on corticosteroid-mediated blood pressure control.

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Main Methods:

  • Review of existing literature on corticosteroid metabolism and blood pressure regulation.
  • Analysis of genetic mutations (e.g., 11beta-HSD2 gene) and their association with hypertension syndromes (e.g., apparent mineralocorticoid excess).
  • Examination of epidemiological data linking gene polymorphisms (HSD11B2) to salt sensitivity and hypertension, and consideration of extrarenal influences.

Main Results:

  • Mutations in the 11beta-HSD2 gene cause apparent mineralocorticoid excess (AME), characterized by severe hypertension and hypokalemia due to cortisol activating the MR.
  • Inhibition of 11beta-HSD2 by substances like liquorice leads to a milder form of AME.
  • Polymorphisms in the HSD11B2 gene are associated with salt sensitivity and predisposition to hypertension.
  • Fetal exposure to glucocorticoids may program for adult hypertension, indicating early programming effects.

Conclusions:

  • 11beta-hydroxysteroid dehydrogenases (11beta-HSDs) are critical regulators of blood pressure by controlling glucocorticoid and mineralocorticoid receptor activation.
  • Dysregulation of 11beta-HSD activity, through genetic or environmental factors, contributes significantly to the pathophysiology of human hypertension.
  • Both central and peripheral actions of corticosteroids, including effects in the vasculature and CNS, alongside early life programming, play roles in blood pressure homeostasis and disease.