Control of outflow resistance by soluble adenylyl cyclase

Yong Suk Lee, Alan D Marmorstein

Research output: Contribution to journalArticle

6 Citations (Scopus)

Abstract

Glaucoma is a leading cause of blindness in the United States affecting as many as 2.2 million Americans. All current glaucoma treatment strategies aim to reduce intraocular pressure, even in patients with normal tension glaucoma. Typically, this is accomplished by reducing the rate of aqueous flow by limiting aqueous production or enhancing drainage using drugs and surgery. Whereas these strategies are effective in diminishing vision loss, some patients continue to lose vision and many discontinue use of their medications because of undesirable side effects. Drugs known to be effective in altering conventional outflow have for the most part been abandoned from modern clinical practice due to undesirable side effects. Identification of new drugs that could enhance conventional outflow, would offer additional options in the treatment of glaucoma and ocular hypertension. To this end, our laboratory has recently uncovered a novel pathway for regulation of conventional outflow by the ciliary body. This pathway is dependent on soluble adenylyl cyclase, an enzyme that catalyzes the generation of cyclic adenosine 3′,5′ monophosphate (cAMP) in response to bicarbonate.

Original languageEnglish (US)
Pages (from-to)138-142
Number of pages5
JournalJournal of Ocular Pharmacology and Therapeutics
Volume30
Issue number2-3
DOIs
StatePublished - Mar 1 2014

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Adenylyl Cyclases
Glaucoma
Pharmaceutical Preparations
Low Tension Glaucoma
Ocular Hypertension
Ciliary Body
Blindness
Bicarbonates
Intraocular Pressure
Adenosine
Drainage
Enzymes
Therapeutics

ASJC Scopus subject areas

  • Pharmacology (medical)
  • Ophthalmology
  • Pharmacology
  • Medicine(all)

Cite this

Control of outflow resistance by soluble adenylyl cyclase. / Lee, Yong Suk; Marmorstein, Alan D.

In: Journal of Ocular Pharmacology and Therapeutics, Vol. 30, No. 2-3, 01.03.2014, p. 138-142.

Research output: Contribution to journalArticle

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