Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3 Pt 2
pubmed:dateCreated
1994-5-19
pubmed:abstractText
Hypovolemia activates reflexes that stimulate secretion of renin and arginine vasopressin (AVP). A large body of evidence, obtained mainly in anesthetized preparations, supports the hypothesis that unloading cardiac receptors stimulates increases in plasma AVP and renin activity (PRA). We have observed significant increases in PRA before any change in either mean arterial pressure (MAP) or pulse pressure in conscious dogs undergoing continuous hemorrhage; however, plasma AVP did not change until there was a significant fall in MAP. These results are compatible with the hypothesis that cardiac receptors cause reflex stimulation of renin but not AVP secretion. The aim of the present study was to test the hypothesis that a decrease in atrial pressure alone is sufficient to stimulate an increase in plasma AVP and PRA. Graded thoracic inferior vena caval constriction (TIVCC) was used to reduce atrial pressure in four steps without altering MAP in conscious dogs. In a fifth step, TIVCC was increased to cause a fall in MAP. A reduction in left atrial pressure (LAP) of 4.2 +/- 0.9 mmHg was accompanied by a significant (P < 0.05) increase in PRA from a control value of 0.4 +/- 0.1 ng angiotensin I (ANG I).ml-1.3 h-1 to 1.1 +/- 0.2 ng ANG I.ml-1.3 h-1 but no change in plasma AVP (from 1.0 +/- 0.1 to 1.2 +/- 0.2 pg/ml) or MAP (from 85 +/- 5 mmHg to 86 +/- 4 mmHg).(ABSTRACT TRUNCATED AT 250 WORDS)
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Mar
pubmed:issn
0002-9513
pubmed:author
pubmed:issnType
Print
pubmed:volume
266
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
R714-21
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1994
pubmed:articleTitle
Renin and vasopressin responses to graded reductions in atrial pressure in conscious dogs.
pubmed:affiliation
Department of Physiology, School of Medicine, University of California, San Francisco 94143.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't