Related Experiment Video

Updated: Jun 1, 2026

In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines
09:57

In Vitro Assays to Evaluate the Migration, Invasion, and Proliferation of Immortalized Human First-trimester Trophoblast Cell Lines

Published on: March 5, 2019

Knockout of the vascular endothelial glucocorticoid receptor abrogates dexamethasone-induced hypertension

Julie E Goodwin1, Junhui Zhang, David Gonzalez

  • 1Section of Nephrology, Department of Pediatrics, Yale University School of Medicine, New Haven, Connecticut 06520-8064, USA. julie.goodwin@yale.edu

Journal of Hypertension
|June 11, 2011
PubMed

Insights

Mice lacking the vascular endothelial glucocorticoid receptor are resistant to high blood pressure caused by glucocorticoids. This suggests the receptor plays a key role in blood pressure regulation and circadian rhythms.

Area of Science:

  • Endocrinology
  • Cardiovascular Physiology
  • Molecular Biology

Background:

  • Glucocorticoid-induced hypertension mechanisms are not fully understood.
  • Emerging evidence suggests vascular effects, not sodium retention, are primary.
  • This study investigates the vasculature's role in glucocorticoid hypertension.

Purpose of the Study:

  • To elucidate the role of the vasculature in glucocorticoid-mediated hypertension.
  • To understand the function of the vascular endothelial glucocorticoid receptor.

Main Methods:

  • Generated a mouse model with tissue-specific knockout of the glucocorticoid receptor in vascular endothelium.
  • Administered dexamethasone to assess hypertension development.
  • Measured blood pressure and arteriolar contractile responses.

Main Results:

  • Mice lacking the vascular endothelial glucocorticoid receptor showed resistance to dexamethasone-induced hypertension (2.7 mmHg vs. 13.1 mmHg increase).
  • Knockout vessels exhibited reduced contractile response to dexamethasone (6.6% vs. 13.4%).
  • Knockout mice partially recovered normal circadian blood pressure rhythms.

Conclusions:

  • The vascular endothelial glucocorticoid receptor is crucial for blood pressure homeostasis.
  • This receptor may function as a peripheral circadian clock.
  • Highlights the receptor's importance in fundamental physiological processes.
Abstract

More Related Videos

Generation of an Immortalized Murine Brain Microvascular Endothelial Cell Line as an In Vitro Blood Brain Barrier Model09:36

Generation of an Immortalized Murine Brain Microvascular Endothelial Cell Line as an In Vitro Blood Brain Barrier Model

Published on: August 29, 2012

Related Concept Videos

Desensitization and Tachyphylaxis01:20

Desensitization and Tachyphylaxis

Tachyphylaxis is described as a rapid decrease in response to a drug after repeated or continuous administration of the same drug dose. It is a phenomenon where the body becomes less responsive to a particular substance or intervention over time, requiring higher doses or stronger interventions to achieve the same effect. It results from adaptive changes in the body's receptors, signaling pathways, or physiological processes that occur in response to prolonged exposure to a stimulus.
Several...
Antihypertensive Drugs: Action of Diuretics01:16

Antihypertensive Drugs: Action of Diuretics

Diuretics are antihypertensive drugs used to treat hypertension resulting from sodium and water retention. Sodium, vital for fluid balance and nerve or muscle function, is regulated by the kidneys through millions of nephrons. Blood enters nephrons via afferent arterioles, which branch into capillaries called glomeruli. These filter blood plasma, allowing water and solutes, like sodium ions, to pass through capillary walls into Bowman's capsule. The filtrate then flows through various tubules...
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...
GPCR Desensitization01:12

GPCR Desensitization

G protein-coupled receptor (GPCR) signaling plays a crucial role in cell functioning. GPCR desensitization is an equally essential process. It allows cells to respond to changing environments and regain sensitivity to new stimuli while preventing unnecessary stimulation when no longer needed. Prolonged exposure to stimuli leads to GPCR desensitization. It involves blocking the receptors from binding and activating additional G proteins. This inhibits activation of downstream effectors, thereby...
Antihypertensive Drugs: Thiazide-Class Diuretics01:15

Antihypertensive Drugs: Thiazide-Class Diuretics

Thiazide diuretics are sulfonamide derivatives featuring a benzothiadiazine ring system in their molecular structure. Based on this structure, thiazide diuretics can be categorized into two groups: thiazide-type and thiazide-like diuretics. Thiazide-type diuretics, including hydrochlorothiazide and chlorothiazide, consist of a benzothiadiazine backbone with an attached sulfonamide group. Thiazide-like diuretics, such as chlorthalidone and indapamide, lack the thiazide ring but demonstrate...
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,...