Linked Life Data

6309689

Source:http://linkedlifedata.com/resource/pubmed/id/6309689

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1983-10-28
pubmed:abstractText
There has been a suspicion on the part of many clinicians and research scientists that intraocular pressure can be regulated by neural and/or humoral influences upon the rate of aqueous humor formation. It has been difficult, if not impossible, to separate specific influences of the central nervous system upon intraocular pressure from vascular induced or other secondary alterations. The past two decades have witnesses a great deal of study of the role of the adrenergic nervous system upon the regulation of intraocular pressure. From the investigations it is possible to formulate an integrated concept that can place years of work and speculation on a firm molecular foundation. The secretory tissue of the eye, the ciliary processes, contain an enzyme receptor complex, comprised by receptor complex, comprised by receptor bound membrane proteins, the catalytic moiety of the enzyme, a guanyl nucleotide regulatory protein (or N protein) and other features. The enzyme can be activated by well known neurohumoral or humoral agents that consist of catecholamines, glycoprotein hormones produced by the hypothalamic pituitary axis, and other related compounds, including placental gonadotropin. These compounds cause the ciliary epithelia to produce cyclic AMP at an accelerated rate. Cyclic AMP, as a second messenger, causes, either directly or indirectly, a decrease in the rate of aqueous humor formation that may be modulated by cofactors. Clinical syndromes fit the experimental data so that an integrated explanation can be given for the reduced intraocular pressure witnessed under certain central nervous system and adrenergic influences. The molecular biology of this concept provides important leads for future investigations that bear directly both upon the regulation of intraocular pressure and upon glaucoma.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jun
pubmed:issn
0165-5701
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
201-12
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1983
pubmed:articleTitle
A major pathway for the regulation of intraocular pressure.
pubmed:publicationType
Journal Article, Review, Research Support, Non-U.S. Gov't