Linked Life Data

10691794

Source:http://linkedlifedata.com/resource/pubmed/id/10691794

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2000-3-27
pubmed:abstractText
Changes in arterial blood pressure (ABP) lead to changes in vascular shear stress. This mechanical stimulus increases cytosolic Ca2+ in endothelial cells, which in turn activates the endothelial isoform of the nitric oxide synthase. The subsequently formed NO reaches the adjacent vascular smooth muscle cells, where it reduces vascular resistance in order to maintain ABP at its initial level. Thus, NO may play an important role as a physiological blood pressure buffer. Previous data on the importance of eNOS for blood pressure control are reviewed with special emphasis on the fact that endogenous nitric oxide can buffer blood pressure variability (BPV) in dogs, rats and mice. In previous studies where all isoforms of the nitric oxide synthase were blocked pharmacologically, increases in blood pressure and variability were observed. Thus, we set out to clarify which isoform of the nitric oxide synthase is responsible for this BPV controlling effect. Hence, blood pressure control was studied in knock-out mice lacking specifically the gene for endothelial nitric oxide synthase with their respective wild-type controls. One day after surgery, under resting conditions, blood pressure was increased by 47 mmHg (P < 0.05), heart rate was lower (-77 beats min-1, P < 0.05), and BPV doubled (P < 0.05). Based on these results, we conclude that chronic blood pressure levels are influenced by eNOS and that there is a blood pressure buffering effect of endogenous nitric oxide which is mediated by the endothelial isoform of the nitric oxide synthase.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0001-6772
pubmed:author
pubmed:issnType
Print
pubmed:volume
168
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
155-60
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed:year
2000
pubmed:articleTitle
Blood pressure control in eNOS knock-out mice: comparison with other species under NO blockade.
pubmed:affiliation
Johannes-Müller-Institut für Physiologie, Humboldt Universität (Charité), Tucholskystr. 2, Berlin, Germany.
pubmed:publicationType
Journal Article, Comparative Study, Research Support, Non-U.S. Gov't