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

Hepatic Drug Excretion: Enterohepatic Cycling

Hepatic Drug Excretion: Enterohepatic Cycling

Enterohepatic cycling involves the active secretion of drugs and their metabolites into the bile via transporters in the canalicular membrane of hepatocytes. This secretion is an integral part of the digestive process, releasing these substances into the gastrointestinal (GI) tract.
Post-release drugs and metabolites can be reabsorbed into the body from the intestine. For conjugated metabolites like glucuronides, reabsorption requires enzymatic hydrolysis by intestinal microflora. This...

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: 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...

Drug Elimination by Renal Route: Tubular Secretion

Drug Elimination by Renal Route: Tubular Secretion

Once the process of glomerular filtration is completed, blood carrying unfiltered drug molecules traverses through efferent arterioles and makes its way into the peritubular capillaries in the proximal tubule. A variety of carriers play a pivotal role in actively secreting drugs from these peritubular capillaries into the tubular fluid. The organic anion transporter transfers acidic drugs, against an electrochemical gradient, from the peritubular capillaries into the renal tubule cells and...

Renal Drug Excretion: Tubular Secretion

Renal Drug Excretion: Tubular Secretion

Active tubular secretion is a robust, energy-demanding process that utilizes carrier systems to transport drugs into renal tubules. The active renal secretion systems include the organic anion transporter (OAT) for weak acids and the organic cation transporter (OCT) for weak bases. Structurally similar drugs can compete for the same transporter, potentially leading to drug accumulation and toxicity. However, this principle can be exploited therapeutically. One example is probenecid (Probalan),...

Hepatic Drug Clearance: Role of Transporters

Hepatic Drug Clearance: Role of Transporters

In the liver and bile canaliculi, influx and efflux transporters modification can influence intrinsic clearance. Transporters play a significant role in moving drugs within liver cells. Elaborate models, such as the Biopharmaceutical Classification System (BCS), are essential to relate transporters to drug disposition. This system categorizes drugs into four classes based on solubility and permeability, providing insights into elimination routes and the effects of transporters following oral...

You might also read

Related Articles

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

Sort by

Same author

Retraction notice to "Nephroprotective potential of Panduratin A against colistin-induced renal injury via attenuating mitochondrial dysfunction and cell apoptosis" [Biomedicine & Pharmacotherapy 148 (2022) 112732].

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2026

Same author

An ultra-rapid response NIR fluorescent probe for in vivo tracking of sulfite dynamic changes.

Spectrochimica acta. Part A, Molecular and biomolecular spectroscopy·2026

Same author

Activation of farnesoid X receptor inhibits TMEM16A-mediated chloride secretion in renal collecting duct cells and retards renal cyst progression.

American journal of physiology. Renal physiology·2026

Same author

Corrigendum to "ASPP-092, a Curcuma comosa diarylheptanoid, inhibits the adipogenic differentiation of human bone marrow-derived mesenchymal stem cells via activation of TGF-β/SMAD2/3 signaling" [Biomed. Pharmacother. 193 (2025) 118884].

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2026

Same author

Erratum to "ASPP-092, a Curcuma comosa diarylheptanoid, inhibits the adipogenic differentiation of human bone marrow-derived mesenchymal stem cells via activation of TGF-β/SMAD2/3 signaling" [Biomed. Pharmacother. 193 (2025) 118884].

Biomedicine & pharmacotherapy = Biomedecine & pharmacotherapie·2026

Same author

Site-1 protease-derived sPRR contributes to renal ischemia-reperfusion injury in mice by promoting macrophage classical activation.

Clinical science (London, England : 1979)·2026

Search research articles

Related Experiment Video

Updated: May 17, 2026

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium

Published on: September 1, 2015

Liver X receptor agonists decrease ENaC-mediated sodium transport in collecting duct cells.

Sunhapas Soodvilai, Zhanjun Jia, Somsak Fongsupa

American Journal of Physiology. Renal Physiology

|October 19, 2012

Summary

This summary is machine-generated.

Liver X receptors (LXRs) regulate metabolism. LXR ligands inhibit epithelial sodium channel (ENaC)-mediated sodium transport in kidney collecting duct cells, suggesting LXRs as a therapeutic target for hypertension.

More Related Videos

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli

Published on: June 27, 2015

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

Published on: November 10, 2011

Related Experiment Videos

Last Updated: May 17, 2026

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium

Implementing Patch Clamp and Live Fluorescence Microscopy to Monitor Functional Properties of Freshly Isolated PKD Epithelium

Published on: September 1, 2015

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli

Single-channel Analysis and Calcium Imaging in the Podocytes of the Freshly Isolated Glomeruli

Published on: June 27, 2015

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

In vivo Liver Endocytosis Followed by Purification of Liver Cells by Liver Perfusion

Published on: November 10, 2011

Area of Science:

Nephrology
Endocrinology
Molecular Biology

Background:

Liver X receptors (LXRs) are key regulators of lipid, fatty acid, and glucose metabolism.
The role of LXRs in renal function, particularly in regulating sodium transport, remains largely unexplored.

Discussion:

LXR agonists T0901317, GW3965, and 22R-hydroxycholesterol reduced amiloride-sensitive sodium transport in M1 collecting duct cells.
This inhibition was associated with increased transepithelial resistance and decreased ENaC mRNA and membrane expression, independent of Na+/K+-ATPase activity.
LXR activation attenuated aldosterone-stimulated sodium transport and inhibited ENaC function in primary collecting duct cells.

Key Insights:

LXR-activating ligands directly modulate ENaC-mediated sodium transport in kidney collecting duct cells.
LXR ligands decrease ENaC abundance and function, impacting sodium reabsorption.
These findings reveal a novel mechanism by which LXRs influence renal sodium handling.

Outlook:

LXRs represent a potential therapeutic target for managing conditions characterized by ENaC dysregulation, such as hypertension.
Further research into LXR-ENaC interactions could uncover new strategies for blood pressure control.
Investigating the precise molecular pathways linking LXR activation to ENaC regulation is warranted.