Search research articles

ABOUT JoVE

Overview Leadership Blog JoVE Help Center

AUTHORS

Publishing Process Editorial Board Scope & Policies Peer Review FAQ Submit

LIBRARIANS

Testimonials Subscriptions Access Resources Library Advisory Board FAQ

RESEARCH

JoVE Journal Methods Collections JoVE Encyclopedia of Experiments Archive

EDUCATION

JoVE Core JoVE Business JoVE Science Education JoVE Lab Manual Faculty Resource Center Faculty Site

Terms & Conditions of Use

Related Concept Videos

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

Heart Failure Drugs: Inhibitors of Renin-Angiotensin System

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...

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Antihypertensive Drugs: Angiotensin-Converting Enzyme Inhibitors

Angiotensin-converting enzyme (ACE), a vital component of the renin-angiotensin-aldosterone system, is abundant in lung endothelial cells. ACE converts the inactive decapeptide, angiotensin I, into the active octapeptide, angiotensin II. This potent vasoconstrictor narrows blood vessels, increasing resistance to blood flow and elevating blood pressure. Angiotensin II also stimulates aldosterone production, encouraging kidney cells to reabsorb more sodium and water from urine, thereby increasing...

Antihypertensive Drugs: Angiotensin II Receptor Blockers

Antihypertensive Drugs: Angiotensin II Receptor Blockers

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...

Antihypertensive Drugs: Vasodilators

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...

Antihypertensive Drugs: Action of Calcium Channel Blockers

Antihypertensive Drugs: Action of Calcium Channel Blockers

Calcium ions are essential to contract smooth muscle cells in blood vessels. They enter these cells through voltage-dependent calcium channels, specifically L-type calcium channels in the cell membrane. These L-type calcium channels are integral to the excitation-contraction coupling process in smooth muscle. When a stimulus is received by smooth muscle cells, their membrane depolarizes. This alteration in membrane potential instigates the opening of L-type calcium channels. As a result,...

Antihypertensive Drugs: Direct Renin Inhibitors

Antihypertensive Drugs: Direct Renin Inhibitors

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,...

You might also read

Related Articles

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

Sort by

Same author

Cardiopulmonary Baroreflex Control of Renal Sympathetic Nerve Activity Is Impaired in Dogs With Left Ventricular Dysfunction.

Journal of cardiac failure·2019

Same author

Does the benefit from treating to lower blood pressure targets vary with age? A systematic review and meta-analysis.

Journal of hypertension·2019

Same author

History and Justification of a National Blood Pressure Measurement Validated Device Listing.

Hypertension (Dallas, Tex. : 1979)·2018

Same author

Hydrochlorothiazide vs chlorthalidone, indapamide, and potassium-sparing/hydrochlorothiazide diuretics for reducing left ventricular hypertrophy: A systematic review and meta-analysis.

Journal of clinical hypertension (Greenwich, Conn.)·2018

Same author

Subcutaneous Furosemide in Heart Failure: Pharmacokinetic Characteristics of a Newly Buffered Solution.

JACC. Basic to translational science·2018

Same author

Hydrochlorothiazide and alternative diuretics versus renin-angiotensin system inhibitors for the regression of left ventricular hypertrophy: a head-to-head meta-analysis.

Journal of hypertension·2018

Search research articles

Related Experiment Video

Updated: Jul 15, 2026

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

Centrally acting antihypertensive agents: an update.

Domenic A Sica¹

¹Division of Nephrology, Medical College of Virginia, Virginia Commonwealth University, Richmond, VA 23298-0160, USA. dsica@hsc.vcu.edu

Journal of Clinical Hypertension (Greenwich, Conn.)

|May 9, 2007

Summary

Centrally acting agents, like clonidine, reduce sympathetic outflow by stimulating specific receptors. These agents are effective for resistant hypertension, especially in patients with diabetes or kidney issues.

Related Experiment Videos

Last Updated: Jul 15, 2026

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Improved Renal Denervation Mitigated Hypertension Induced by Angiotensin II Infusion

Published on: May 26, 2022

Area of Science:

Pharmacology
Cardiovascular Medicine
Neuroscience

Background:

Centrally acting agents target alpha(2) and/or imidozoline receptors in the rostral ventrolateral medulla.
These agents reduce sympathetic nervous system outflow, impacting blood pressure regulation.
Alpha-methyldopa, an early central alpha agonist, has seen reduced use due to side effects.

Purpose of the Study:

To review the mechanisms, clinical applications, and limitations of centrally acting antihypertensive agents.
To highlight their utility in specific patient populations and perioperative settings.
To discuss adjunctive therapies and potential risks.

Main Methods:

Review of existing literature on centrally acting antihypertensive agents.
Analysis of receptor interactions and downstream effects on sympathetic outflow.
Examination of clinical trial data and case reports regarding efficacy and safety.

Main Results:

Central alpha agonists effectively lower blood pressure, particularly in resistant hypertension, diabetes, and renal failure.
Clonidine demonstrates efficacy in perioperative hypertension and may reduce anesthesia/analgesia requirements.
Sustained-release moxonidine use in heart failure is linked to increased mortality and morbidity.

Conclusions:

Centrally acting agents remain valuable for specific hypertensive conditions, especially when combined with other therapies.
Careful patient selection and monitoring are crucial, considering potential side effects like salt and water retention.
Diuretic therapy is often necessary as an adjunct to manage fluid retention associated with escalating doses.