Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1969-6-29
pubmed:keyword
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0003-4819
pubmed:author
pubmed:issnType
Print
pubmed:volume
70
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1033-8
pubmed:dateRevised
2009-10-27
pubmed:otherAbstract
PIP: Substantial evidence has accumulated that the prostaglandins A (PGA) compounds, potent naturally occurring renal antihypertensive agents, may function as circulating renal vasodilators and may be responsible at least in part for the antihypertensive function of the kidney. The concept that essential hypertension is not solely the result of increased renal pressure mechanisms but may be a deficiency disorder of renal vasodepressor agents has been reinforced with isolation from the kidney of the naturally occurring peripheral vasodilator, PGA2. Along with its possible role in essential hypertension, PGA2 might function as a natriuretic "hormone." All available data indicate that the renal response to prostaglandin infusion in animals and humans with essential hypertension is characterized by an increase in cortical blood flow, glomerular filtration rate, sodium and potassium excretion, urine flow, and free-water clearance. Of all the prostaglandins investigated thus far, the most promising compounds from a cardiovascular-renal perspective are the PGA class. From their highly desirable mechanism of antihypertension and natriuretic action, the greatest immediate potential for PGA1 and PGA2 is for pharmacological use in the treatment of such disorders as hypertension and edema.
pubmed:meshHeading
pubmed:year
1969
pubmed:articleTitle
Hypertension, natriuresis, and the renal prostaglandins.
pubmed:publicationType
Journal Article