Linked Life Data

16141376

Source:http://linkedlifedata.com/resource/pubmed/id/16141376

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-12-16
pubmed:abstractText
The early (approximately 30 min) postexercise hypotension response after a session of aerobic exercise is due in part to H1-receptor-mediated vasodilation. The purpose of this study was to determine the potential contribution of H2-receptor-mediated vasodilation to postexercise hypotension. We studied 10 healthy normotensive men and women (ages 23.7 +/- 3.4 yr) before and through 90 min after a 60-min bout of cycling at 60% peak O2 uptake on randomized control and H2-receptor antagonist days (300 mg oral ranitidine). Arterial pressure (automated auscultation), cardiac output (acetylene washin) and femoral blood flow (Doppler ultrasound) were measured. Vascular conductance was calculated as flow/mean arterial pressure. Sixty minutes postexercise on the control day, femoral (delta62.3 +/- 15.6%, where Delta is change; P < 0.01) and systemic (delta13.8 +/- 5.3%; P = 0.01) vascular conductances were increased, whereas mean arterial pressure was reduced (Delta-6.7 +/- 1.1 mmHg; P < 0.01). Conversely, 60 min postexercise with ranitidine, femoral (delta9.4 +/- 9.2%; P = 0.34) and systemic (delta-2.8 +/- 4.8%; P = 0.35) vascular conductances were not elevated and mean arterial pressure was not reduced (delta-2.2 +/- 1.3 mmHg; P = 0.12). Furthermore, postexercise femoral and systemic vascular conductances were lower (P < 0.05) and mean arterial pressure was higher (P = 0.01) on the ranitidine day compared with control. Ingestion of ranitidine markedly reduces vasodilation after exercise and blunts postexercise hypotension, suggesting H2-receptor-mediated vasodilation contributes to postexercise hypotension.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
8750-7587
pubmed:author
pubmed:issnType
Print
pubmed:volume
100
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
67-75
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
2006
pubmed:articleTitle
H2-receptor-mediated vasodilation contributes to postexercise hypotension.
pubmed:affiliation
Department of Human Physiology, 122 Esslinger Hall, 1240 University of Oregon, Eugene, Oregon 97403-1240, USA.
pubmed:publicationType
Journal Article, Randomized Controlled Trial, Research Support, Non-U.S. Gov't, Research Support, N.I.H., Extramural