Related Experiment Video

Updated: Jul 11, 2026

Generation of an Immortalized Murine Brain Microvascular Endothelial Cell Line as an In Vitro Blood Brain Barrier Model
09:36

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

Published on: August 29, 2012

Acute effects of glucocorticoids on endothelial fibrinolytic and vasodilator function in humans

Anna R Dover1, Patrick W F Hadoke, Brian R Walker

  • 1Centre for Cardiovascular Science, University of Edinburgh, Edinburgh, Scotland, UK. anna.dover@ed.ac.uk

Journal of Cardiovascular Pharmacology
|September 20, 2007
PubMed

Insights

Short-term cortisol variations do not impact endothelial function. This study found that glucocorticoids do not acutely affect fibrinolytic or vasomotor capacity in healthy individuals, suggesting no immediate link to morning coronary events.

Area of Science:

  • Cardiovascular Physiology
  • Endocrinology
  • Thrombosis Research

Background:

  • Acute coronary events often occur in the morning, coinciding with low fibrinolytic activity and high cortisol levels.
  • Chronic glucocorticoid excess is linked to prothrombotic states and endothelial dysfunction, suggesting a potential role in cardiovascular events.

Purpose of the Study:

  • To investigate the hypothesis that glucocorticoids impair endothelial fibrinolytic capacity.
  • To determine the acute effects of short-term variations in plasma cortisol on endothelial fibrinolytic and vasomotor function in healthy subjects.

Main Methods:

  • Twelve healthy volunteers participated in three sessions involving metyrapone and hydrocortisone or saline infusions.
  • Forearm blood flow and fibrinolytic indices were measured using venous occlusion plethysmography during intrabrachial infusions of bradykinin, acetylcholine, and sodium nitroprusside.

Main Results:

  • Hydrocortisone administration did not alter systemic concentrations of plasminogen activator inhibitor type 1 (PAI-1) or tissue plasminogen activator (t-PA).
  • Bradykinin-induced increases in plasma t-PA and forearm blood flow were not affected by systemic hydrocortisone.
  • Endothelial responses to acetylcholine and sodium nitroprusside remained unchanged following hydrocortisone infusion.

Conclusions:

  • Short-term fluctuations in plasma cortisol within the physiological range do not acutely affect endothelial fibrinolytic or vasomotor function in humans.
  • Glucocorticoids do not appear to exert acute in vivo effects on endothelial function, challenging the proposed link to morning circadian variations in coronary events.

More Related Videos

Assessing Endothelial Vasodilator Function with the Endo-PAT 200007:46

Assessing Endothelial Vasodilator Function with the Endo-PAT 2000

Published on: October 15, 2010

Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research08:42

Ultrasound Assessment of Endothelial-Dependent Flow-Mediated Vasodilation of the Brachial Artery in Clinical Research

Published on: October 22, 2014

Related Concept Videos

Acute Inflammation III: Local and Systemic Effects01:25

Acute Inflammation III: Local and Systemic Effects

Acute inflammation produces a coordinated set of local and systemic changes that limit injury, eliminate pathogens, and initiate repair. These responses arise within minutes of infection, trauma, or chemical insult and are driven by vascular alterations and leukocyte-derived mediators. When the stimulus resolves, the reaction typically abates within days.Local EffectsAt the site of injury, arteriolar vasodilation increases blood flow, resulting in redness and warmth. Simultaneously, increased...
Clot Retraction and Fibrinolysis01:16

Clot Retraction and Fibrinolysis

After a fibrin clot is formed, the next step is clot retraction, a vital process facilitated by platelet contractile proteins, such as actin and myosin. These proteins pull the fibrin strands closer together and condense the clot. This action reduces the size of the clot, creating a smaller, denser structure that effectively seals off the damaged vessel. Clot retraction consolidates the clot and helps with wound healing by bringing the edges of the damaged blood vessel closer together.
Anticoagulant Drugs: Low-Molecular-Weight Heparins01:30

Anticoagulant Drugs: Low-Molecular-Weight Heparins

Hemostasis is a crucial process that prevents excessive blood loss from damaged blood vessels. It involves various mechanisms such as vasoconstriction, platelet adhesion and activation, and fibrin formation. The importance of each mechanism depends on the type of vessel injury. In contrast, thrombosis is the abnormal formation of a blood clot within the blood vessels, leading to potential complications if the clot obstructs blood flow. Thrombosis can be caused by increased coagulability of the...
Heart Failure Drugs: β-Blockers01:22

Heart Failure Drugs: β-Blockers

β-adrenergic antagonists, commonly known as β-blockers, block the effects of sympathetic neurotransmitters such as noradrenaline (NA) and adrenaline (ADR). They have several beneficial effects in heart failure treatment. They reduce heart rate, the force of contraction, and cardiac muscle relaxation. They also slow the atrial-ventricular conduction rate and raise the threshold for arrhythmias. The concentration of β-blockers determines their effects on bronchodilation, vasodilation, and...
Antihypertensive Drugs: Vasodilators01:23

Antihypertensive Drugs: Vasodilators

Vasodilators, primarily affecting the smooth muscles within arterial and venous walls, are commonly used for hypertension treatment. Medications such as minoxidil and hydralazine primarily target arteries and arterioles, while sodium nitroprusside acts on arterioles and venules. Minoxidil, functioning as a prodrug, is metabolized by hepatic sulfotransferase into its active form, minoxidil sulfate, after oral administration. This metabolite binds to the sulfonylurea receptor (SUR) component of...