Journal article
Role of cyclooxygenase metabolites in mediating platelet-induced baroreceptor dysfunction
American journal of physiology. Heart and circulatory physiology, Vol.269(2), pp.H599-H608
08/01/1995
DOI: 10.1152/ajpheart.1995.269.2.H599
PMID: 7653624
Abstract
The goal of the study was to determine the role of cyclooxygenase metabolites in mediating platelet-induced suppression of baroreceptor activity. Exposure of the isolated carotid sinus of rabbits to thrombin-activated rabbit platelets (3 x 10(8) cells/ml Krebs buffer) decreased baroreceptor activity (P < 0.05) without significantly altering the slope of the pressure-activity relation (gain). The platelet-induced suppression of activity was not blocked but instead was even more pronounced after inhibition of cyclooxygenase with indomethacin; both maximum baroreceptor activity and gain were decreased markedly. The exacerbation of platelet-induced baroreceptor dysfunction contrasted with equivalent carotid vasoconstrictor responses to platelets before and after indomethacin. Furthermore, the stable thromboxane (TxA2) mimetic U-46619 caused similar vasoconstriction as platelets but did not influence baroreceptor gain or maximum activity. In contrast to indomethacin, the selective TxA2 synthesis inhibitor and receptor blocker CGS-22652 failed to influence platelet-induced suppression of activity. In summary, 1) rabbit platelet aggregating in carotid sinus suppress baroreceptor activity, which cannot be explained by the vasoconstriction, and 2) the suppression of activity is not mediated by TxA2 from platelets and is opposed by prostacyclin (PGI2) or other prostanoids produced in carotid sinus. The combination of impaired formation of PGI2 and platelet activation in atherosclerotic and thrombotic states may lead to profound baroreceptor dysfunction.
Details
- Title: Subtitle
- Role of cyclooxygenase metabolites in mediating platelet-induced baroreceptor dysfunction
- Creators
- Zhi Li - University of IowaXin Su - Department of Internal Medicine, University of Iowa College ofMedicine, Iowa City 52242, USAMark W Chapleau - Department of Internal Medicine, University of Iowa College ofMedicine, Iowa City 52242, USA
- Resource Type
- Journal article
- Publication Details
- American journal of physiology. Heart and circulatory physiology, Vol.269(2), pp.H599-H608
- DOI
- 10.1152/ajpheart.1995.269.2.H599
- PMID
- 7653624
- ISSN
- 0363-6135
- eISSN
- 1522-1539
- Language
- English
- Date published
- 08/01/1995
- Academic Unit
- Molecular Physiology and Biophysics; Cardiovascular Medicine; Internal Medicine
- Record Identifier
- 9984025424302771
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