Endothelin1 and Nitric Oxide Synthase: Role in Glaucoma

Ganesh Prasanna, PhD
Univ. of North Texas Health Science (Fort Worth, TX)
Year Awarded:
2000
Grant Duration:
April 1, 2000 to March 31, 2002
Disease:
Glaucoma
Award Amount:
$60,000
Grant Reference ID:
G2000006
Award Type:
Standard
Award Region:
US Southern

Endothelin1 and Nitric Oxide Synthase: Role in Glaucoma

Details


Endothelin-1 (ET-1) is a small peptide molecule that causes blood vessels to constrict. It is elevated in the aqueous humor of people with primary open angle glaucoma and in the blood plasma of people with normal tension glaucoma. Chronic low-dose administration of the peptide to primates produces optic nerve damage that mirrors the damage found in glaucoma. ET-1 may also regulate another vessel-constricting molecule called nitric oxide (NO). The excess production of NO, through enzymes called NO synthases (NOS), in ocular cells also causes optic nerve damage. It has been found that in rats with glaucoma, inhibitors of the NOS-2 enzyme prevent damage to the retinal ganglion cells. In earlier research, Dr. Prasanna found evidence that ET-1 increases the amount of NOS-2 in human pigmented ciliary epithelial cells, and is now utilizing the rat model of glaucoma to examine the role of ET-1 in regulating NOS-2 gene expression. The knowledge gained from this study could help provide a basis for the use of molecules that inhibit the activity of ET-1 as a possible treatment of glaucoma.

Publications

Yorio, T., Krishnamoorthy, T., and Prasanna, G. (2002) Endothelin: is it a contributor to glaucoma pathophysiology? Journal of Glaucoma. 11:259-270.  

Don't miss out.
Receive research updates, inspiring stories, and expert advice
Please enter your first name.
Please enter your last name.
Keep me informed about: *
Please select at least one.
You must select at least one disease category.