Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System01:26

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

671
The activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS) contributes to cardiac remodeling, and inhibiting the RAAS is a pharmacological target in heart failure management. As a result, neurohumoral modulation is a crucial treatment principle for managing heart failure. This approach involves using medications like ACE inhibitors (ACEIs), angiotensin receptor blockers (ARBs), β-blockers, mineralocorticoid receptor antagonists (MRAs), and neutral...
671
Antihypertensive Drugs: Direct Renin Inhibitors01:25

Antihypertensive Drugs: Direct Renin Inhibitors

1.0K
The renin-angiotensin-aldosterone system (RAAS) is an intricate physiological pathway involving numerous enzymes and hormones, including renin, angiotensin-converting enzyme (ACE), angiotensin I and II, and aldosterone. Imbalances within this system increase the production of angiotensin II and aldosterone. Increased angiotensin II levels promote vasoconstriction and blood pressure elevation. Concurrently, higher aldosterone levels stimulate sodium and water reabsorption in the kidneys,...
1.0K
Antihypertensive Drugs: Potassium-Sparing Diuretics01:28

Antihypertensive Drugs: Potassium-Sparing Diuretics

1.9K
Liddle syndrome is a genetically inherited form of hypertension characterized by the overactivity of epithelial sodium channels in the nephron, the functional unit of the kidney. This heightened activity leads to increased sodium reabsorption and excessive excretion of potassium. To counteract this, potassium-sparing diuretics such as amiloride are used. They function by blocking these sodium channels, thereby reducing the influx of sodium into the epithelial cells and minimizing the loss of...
1.9K
Antihypertensive Drugs: Angiotensin II Receptor Blockers01:30

Antihypertensive Drugs: Angiotensin II Receptor Blockers

2.1K
In the renin-angiotensin-aldosterone system, a hormone called angiotensin II plays a crucial role. It binds to the AT1 receptors in vascular smooth muscles coupled with Gq proteins. The activation of these receptors activates an enzyme called phospholipase C, which releases two molecules: inositol trisphosphate and diacylglycerol. These molecules cause a chain reaction that leads to the phosphorylation of myosin light chains and promotes interaction between actin and myosin, leading to smooth...
2.1K
Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers01:22

Adrenergic Antagonists: Pharmacological Actions of ɑ-Receptor Blockers

1.2K
α-Adrenergic antagonists, known as α-blockers, exert their effects by inhibiting α-adrenoceptors, leading to specific physiological actions. α1-blockers and α2-blockers have distinct pharmacological actions and therapeutic applications.
α1-blockers: These drugs inhibit α1-adrenoceptors on smooth muscle cells, resulting in vasodilation. This vasodilation lowers blood pressure, making α1-blockers valuable in treating hypertension. Additionally,...
1.2K
Antihypertensive Drugs: Action of β1 Blockers01:17

Antihypertensive Drugs: Action of β1 Blockers

1.7K
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,...
1.7K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Primary aldosteronism.

Nature reviews. Disease primers·2026
Same author

Barriers for Secondary Hypertension Screening in the United States: A National Physician Survey.

Journal of the American Heart Association·2026
Same author

Expression status of neurotrophic tropomyosin receptor kinase (NTRK1) in pheochromocytoma and its association with clinicopathological factors.

Histology and histopathology·2026
Same author

Aldosterone Synthase Expression vs. Cross-Sectional Imaging in Lateralized Primary Aldosteronism.

The Journal of clinical endocrinology and metabolism·2026
Same author

Modest Contribution of Bradykinin to Blood Pressure Reduction by Sacubitril/Valsartan in Chronic Heart Failure.

Circulation. Heart failure·2026
Same author

Docetaxel-Induced Immune Activation Shows Antitumor Synergy With the Tumor-Targeted CD40 Agonist KK2269.

Cancer science·2026
Same journal

Tirzepatide versus conventional GLP-1 receptor agonists for treatment simplification in type 2 diabetes mellitus: a real-world study.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists·2026
Same journal

Risk-stratification of pediatric thyroid nodules using ATA and ACR TIRADS adult thyroid nodule scoring systems.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists·2026
Same journal

Effectiveness of GLP-1 receptor agonists and SGLT-2 inhibitors combination therapy in type 2 diabetes: a real world experience.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists·2026
Same journal

North American Society for Interventional Thyroidology (NASIT) Statement on Directed Ablative Therapy for the Management of of Low Risk Papillary Thyroid Carcinoma.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists·2026
Same journal

Lower Cutoffs Improve the Diagnostic Performance of DDAVP-Stimulated Bilateral Inferior Petrosal Sinus Sampling for Cushing Disease: A Prospective Cohort Study.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists·2026
Same journal

Efficacy of Initiation of Semaglutide versus SGLT2 inhibitors in Metabolic Dysfunction-Associated Steatotic Liver Disease (MASLD): A Multicenter Propensity-Matched Real-World Study.

Endocrine practice : official journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists·2026
See all related articles

Related Experiment Video

Updated: Nov 20, 2025

A Novel Method: Super-selective Adrenal Venous Sampling
06:08

A Novel Method: Super-selective Adrenal Venous Sampling

Published on: September 15, 2017

23.9K

Mineralocorticoid Receptor Antagonists Decrease the Rates of Positive Screening for Primary Aldosteronism.

Yuta Tezuka1, Adina F Turcu2

  • 1From the (1)Division of Metabolism, Endocrinology and Diabetes, University of Michigan, Ann Arbor, Michigan, and; Division of Nephrology, Endocrinology and Vascular Medicine, Tohoku University Graduate School of Medicine, Sendai, Miyagi, Japan.

Endocrine Practice : Official Journal of the American College of Endocrinology and the American Association of Clinical Endocrinologists
|January 20, 2021
PubMed
Summary
This summary is machine-generated.

Mineralocorticoid receptor antagonists (MRAs) can alter primary aldosteronism (PA) screening results by decreasing the aldosterone/renin ratio (ARR). Repeat PA screening off MRAs when suspected for accurate diagnosis.

More Related Videos

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

10.3K
A Chemical Screening Procedure for Glucocorticoid Signaling with a Zebrafish Larva Luciferase Reporter System
13:22

A Chemical Screening Procedure for Glucocorticoid Signaling with a Zebrafish Larva Luciferase Reporter System

Published on: September 10, 2013

12.2K

Related Experiment Videos

Last Updated: Nov 20, 2025

A Novel Method: Super-selective Adrenal Venous Sampling
06:08

A Novel Method: Super-selective Adrenal Venous Sampling

Published on: September 15, 2017

23.9K
Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice
07:36

Induction of Atherosclerotic Plaques Through Activation of Mineralocorticoid Receptors in Apolipoprotein E-deficient Mice

Published on: September 26, 2018

10.3K
A Chemical Screening Procedure for Glucocorticoid Signaling with a Zebrafish Larva Luciferase Reporter System
13:22

A Chemical Screening Procedure for Glucocorticoid Signaling with a Zebrafish Larva Luciferase Reporter System

Published on: September 10, 2013

12.2K

Area of Science:

  • Endocrinology
  • Hypertension Management
  • Clinical Diagnostics

Background:

  • Mineralocorticoid receptor antagonists (MRAs) are crucial for managing resistant hypertension and primary aldosteronism (PA).
  • PA screening ideally requires medication cessation, posing challenges in patients with severe hypertension or hypokalemia.
  • The impact of MRAs on PA screening in clinical practice remains to be fully elucidated.

Purpose of the Study:

  • To evaluate the effect of MRAs on primary aldosteronism (PA) screening parameters in a clinical setting.
  • To assess how MRA use influences the aldosterone/renin ratio (ARR) and screening test results.
  • To determine the implications for PA diagnostic strategies when patients are on MRAs.

Main Methods:

  • Retrospective cohort study of hypertensive patients undergoing plasma aldosterone and renin measurements.
  • Analysis of data from a tertiary referral center over 19 years, including patients before and after MRA initiation.
  • Assessment of changes in plasma aldosterone, renin, and ARR, and their correlation with MRA treatment duration and other antihypertensives.

Main Results:

  • MRAs significantly increased plasma renin and aldosterone levels, while decreasing the aldosterone/renin ratio (ARR) (P<.0001).
  • Nearly half (48%) of patients showed abrogated positive PA screening after MRA initiation.
  • Conversely, 17% exhibited positive screening only after MRA treatment, often due to hypokalemia correction; high MRA doses and beta-blocker use influenced screening persistence.

Conclusions:

  • Mineralocorticoid receptor antagonists (MRAs) frequently reduce the aldosterone/renin ratio (ARR), potentially masking or altering primary aldosteronism (PA) screening results.
  • When primary aldosteronism is suspected, it is recommended to repeat screening after discontinuing MRAs for accurate diagnosis.
  • Clinical practice should consider the confounding effects of MRAs on PA screening assays.