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

Open Angle Glaucoma: Treatment

Open Angle Glaucoma: Treatment

In open-angle glaucoma, the iridocorneal angle remains open, but the trabecular meshwork becomes stiff, slowing down the outflow of aqueous humor. This causes a buildup of aqueous humor in the anterior chamber, leading to a sudden increase in intraocular pressure. The treatment for open-angle glaucoma focuses on reducing the elevated intraocular pressure by either decreasing the secretion of aqueous humor or increasing its outflow.
Drugs such as carbonic anhydrase inhibitors, α2- and...

G-Protein Gated Ion Channels

G-Protein Gated Ion Channels

GPCRs are primarily responsible for our sense of smell, taste, and vision. The binding of a sensory stimulus activates GPCR to stimulate effector proteins, many of which are ion channels in the sensory organs. GPCRs modulate the opening and closing of the target ion channels either directly by binding them, or by releasing second messengers that activate these channels. As ions move across the membrane, the membrane potential is altered, which induces an appropriate response.
Sensory organs,...

GPCRs Regulate Adenylyl Cylase Activity

GPCRs Regulate Adenylyl Cylase Activity

Some GPCRs transmit signals through adenylyl cyclase (AC), a transmembrane enzyme. AC helps synthesize second messenger cyclic adenosine monophosphate (cAMP). AC catalyzes cyclization reaction and converts ATP to cAMP by releasing a pyrophosphate. The pyrophosphate is further hydrolyzed to phosphate by the enzyme pyrophosphatase, which drives cAMP synthesis to completion. However, cAMP is rapidly degraded to 5′ AMP by the enzymes phosphodiesterase (PDE), preventing overstimulation of cells.
Two...

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,...

Feedback Regulation of Calcium Concentration

Feedback Regulation of Calcium Concentration

Calcium is an essential signaling molecule required for various cellular functions. Calcium pumps and ion channels on cell and organellar membranes, such as those on the endoplasmic reticulum (ER), regulate calcium concentrations inside the cell. They remain closed, keeping the cytosolic calcium levels low at a resting state.
Various transmembrane receptors, such as G protein-coupled receptors (GPCRs), elicit a response to extracellular signals by increasing cytosolic calcium. Activated GPCRs...

Overview of Secretory Vesicles

Overview of Secretory Vesicles

Secretory vesicles, also known as dense core vesicles (DCVs), are membrane-bound vesicles that transport secretory proteins, such as hormones or neurotransmitters. Regulated secretory vesicles transport proteins from the trans-Golgi network to the exterior of the cell. Proteins present in regulated secretory vesicles are required to be rapidly exocytosed in large amounts upon a specific stimulus.
Various proteins regulate the aggregation of molecules inside the secretory vesicles. Chromogranins...

You might also read

Related Articles

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

Sort by

Same author

Relaxation of Precontracted Ciliary Artery and Ciliary Muscle <i>In Vitro</i> by Kinin Peptides: Relevance to Retinal Blood Flow and Intraocular Pressure Regulation.

Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics·2025

Same author

Cutamesine (SA4503) Protects Retinal Ganglion Cells in an Ocular Hypertension Model of Glaucoma Determined Using Detection of Apoptosing Retinal Cells Technology and RBPMS Cell Marker.

Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics·2025

Same author

Posterior Ciliary Artery Contraction by Bradykinin Receptor Subtypes and Implications for Retinal Blood Flow Dysfunction.

Frontiers in bioscience (Elite edition)·2025

Same author

Safety and efficacy of MCO-010 optogenetic therapy in patients with Stargardt disease in USA (STARLIGHT): an open-label multi-center Ph2 trial.

EClinicalMedicine·2025

Same author

Felodipine re-positioned as a neuroprotectant via improved optic nerve head blood circulation in retinal ischemic rabbits and ocular hypertensive rats.

Scientific reports·2025

Same author

Consensus Recommendations for Studies of Outflow Facility and Intraocular Pressure Regulation Using Ex Vivo Perfusion Approaches.

Investigative ophthalmology & visual science·2024

Search research articles

Related Experiment Video

Updated: Jun 25, 2026

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells

Published on: July 16, 2013

Human trabecular meshwork cell volume decrease by NO-independent soluble guanylate cyclase activators YC-1 and

William M Dismuke¹, Najam A Sharif, Dorette Z Ellis

¹Department of Pharmacodynamics, College of Pharmacy, University of Florida, Gainesville, Florida 32610, USA.

Investigative Ophthalmology & Visual Science

|February 24, 2009

Summary

Nitric oxide-independent activators of soluble guanylate cyclase (sGC) decrease trabecular meshwork (TM) cell volume, increasing aqueous humor outflow. This involves the sGC/cGMP/PKG pathway and potassium ion (K+) efflux.

More Related Videos

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Published on: June 20, 2015

Preparation and Utilization of Freshly Isolated Human Detrusor Smooth Muscle Cells for Characterization of 9-Phenanthrol-Sensitive Cation Currents

Preparation and Utilization of Freshly Isolated Human Detrusor Smooth Muscle Cells for Characterization of 9-Phenanthrol-Sensitive Cation Currents

Published on: January 31, 2020

Related Experiment Videos

Last Updated: Jun 25, 2026

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells

Mechanical Stimulation-induced Calcium Wave Propagation in Cell Monolayers: The Example of Bovine Corneal Endothelial Cells

Published on: July 16, 2013

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Trabecular Meshwork Response to Pressure Elevation in the Living Human Eye

Published on: June 20, 2015

Preparation and Utilization of Freshly Isolated Human Detrusor Smooth Muscle Cells for Characterization of 9-Phenanthrol-Sensitive Cation Currents

Preparation and Utilization of Freshly Isolated Human Detrusor Smooth Muscle Cells for Characterization of 9-Phenanthrol-Sensitive Cation Currents

Published on: January 31, 2020

Area of Science:

Ophthalmology
Cell Biology
Pharmacology

Background:

Trabecular meshwork (TM) cell volume influences aqueous humor outflow.
Decreasing TM cell volume can enhance aqueous humor outflow.
Nitric oxide (NO)-independent activators of soluble guanylate cyclase (sGC) are potential modulators of TM cell volume.

Purpose of the Study:

To investigate the effects of NO-independent sGC activators, YC-1 and BAY-58-2667, on TM cell volume.
To elucidate the signal transduction pathways and ion channels involved in this regulation.

Main Methods:

TM cell volume was measured using calcein AM dye and confocal microscopy.
Inhibitors and activators of sGC, cyclic guanosine monophosphate (cGMP), protein kinase G (PKG), and BK(Ca) channels were employed.
cGMP levels were quantified using enzyme immunoassay.

Main Results:

YC-1 and BAY-58-2667 exhibited biphasic effects on TM cell volume, initially increasing and then decreasing it at higher concentrations.
The YC-1-induced decrease in cell volume was mediated by sGC, cGMP, PKG, and BK(Ca) channels.
The BAY-58-2667-induced decrease involved PKG and BK(Ca) channels, with sGC inhibition potentiating the effect.

Conclusions:

NO-independent activation of sGC leads to a decrease in TM cell volume.
This process is mediated by the sGC/cGMP/PKG signaling pathway.
Potassium ion (K+) efflux is implicated in the observed TM cell volume reduction.