Linked Life Data

539444

Source:http://linkedlifedata.com/resource/pubmed/id/539444

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
3
pubmed:dateCreated
1980-5-14
pubmed:abstractText
Studies were made of the responses of the vascular bed of cat hind leg to intraarterial injection of noradrenaline, angiotensine, tyramine and vasopressine, as well as of carotid occlusion upon increasing the tissue osmolarity through intraarterial hypertonic infusion. The limb was perfused at constant blood flow. Hyperosmolarity inhibited the contractile effects of all stimuli studied. The inhibition of the contractility was greater in the case of tyramine and identical in the case of the remaining vasoconstrictor agents. Increased KCl content or the addition of L-ascorbic acid to the hypertonic solution with preservation of the same hyperosmolarity reduced the inhibition of the contractile responses to noradrenaline and angiotensine. The restoration of the contractility was much more pronounced upon simultaneous increase in the KCl content and addition of L-ascorbic acid. No recovery of the contractile effect of tyramine was observed. The mechanism of hyperosmolarity inhibition of the vascular contraction is discussed. In all vasoconstrictor stimuli the inhibition is connected primarily with disruption of the transmembrane exchange of Na+ and Ka+. In some vasoconstrictor agents, e. g. tyramine, there is disturbance in the specific mechanism connected secondarily with vascular contraction.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0323-9950
pubmed:author
pubmed:issnType
Print
pubmed:volume
5
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
11-8
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
1979
pubmed:articleTitle
Mechanism of hyperosmolarity inhibition of vascular contractility.
pubmed:publicationType
Journal Article, In Vitro