Endogenous regulation of human Schlemm's canal cell volume by nitric oxide signaling.

Purpose: There is a time-course correlation between nitric oxide (NO)-induced decreases in trabecular meshwork (TM) cell volume and NO-induced increases in outflow facility. The Schlemm's canal (SC) cells may also provide resistance to aqueous humor outflow; therefore, this study tests the involvement of the nitric oxide synthase (NOS) and NO signaling pathway and the BK(Ca)-channel in mediating SC cell volume decreases.

Methods: Cell volume was measured in low-passage human SC cells using calcein AM fluorescent dye; images were captured with a confocal microscope, and data were quantified using NIH ImageJ software.

Activation of the BK(Ca) channel increases outflow facility and decreases trabecular meshwork cell volume.

Purpose: Inhibition of the BK(Ca) channel attenuated the nitric oxide-induced increase in outflow facility and decrease in trabecular meshwork (TM) cell volume suggesting the involvement of the BK(Ca) channel in TM cell function. This study examined the effects of activation of the BK(Ca) channel on outflow facility and TM cell volume and determined if the effects of NO and BK(Ca) channel activation on TM cell volume were additive.

Methods: Porcine eyes were used to measure outflow facility using the anterior segment organ culture perfusion system.

Human trabecular meshwork cell volume decrease by NO-independent soluble guanylate cyclase activators YC-1 and BAY-58-2667 involves the BKCa ion channel.

Purpose: There is a correlation between cell volume changes and changes in the rate of aqueous humor outflow; agents that decrease trabecular meshwork (TM) cell volume increase the rate of aqueous humor outflow. This study investigated the effects of the nitric oxide (NO)-independent activators of soluble guanylate cyclase (sGC), YC-1, and BAY-58-2667 on TM cell volume and the signal transduction pathways and ion channel involved.

Methods: Cell volume was measured with the use of calcein AM fluorescent dye, detected by confocal microscopy.

Characterization of soluble guanylate cyclase in NO-induced increases in aqueous humor outflow facility and in the trabecular meshwork.

Purpose: Nitric oxide (NO) increases the rate at which aqueous humor exits the eye; however, the involvement of soluble guanylate cyclase (sGC) is unknown. This study investigated the role of sGC in mediating the NO-induced increases in outflow facility.

Methods: Outflow facility was measured in porcine eyes using the anterior segment organ culture perfusion system.

NO-induced regulation of human trabecular meshwork cell volume and aqueous humor outflow facility involve the BKCa ion channel.

Nitric oxide (NO) donors decrease intraocular pressure (IOP) by increasing aqueous outflow facility in the trabecular meshwork (TM) and/or Schlemm's canal. However, the cellular mechanisms are unknown. Cellular mechanisms known to regulate outflow facility include changes in cell volume and cellular contractility.