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Titolo:
ROLE OF CYCLOOXYGENASE METABOLITES IN MEDIATING PLATELET-INDUCED BARORECEPTOR DYSFUNCTION
Autore:
LI Z; SU X; CHAPLEAU MW;
Indirizzi:
UNIV IOWA,GEN HOSP,COLL MED,E327,200 HAWKINS DR IOWA CITY IA 52242 UNIV IOWA,COLL MED,DEPT INTERNAL MED IOWA CITY IA 52242 UNIV IOWA,COLL MED,CTR CARDIOVASC IOWA CITY IA 52242 DEPT VET AFFAIRS MED CTR IOWA CITY IA 52246
Titolo Testata:
American journal of physiology. Heart and circulatory physiology
fascicolo: 2, volume: 38, anno: 1995,
pagine: 599 - 608
SICI:
0363-6135(1995)38:2<599:ROCMIM>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
CAROTID-SINUS BARORECEPTORS; AGGREGATING HUMAN-PLATELETS; ARTERIAL BARORECEPTORS; ENDOTHELIAL-CELLS; RABBITS; PROSTACYCLIN; STIMULATION; PROSTAGLANDINS; NOREPINEPHRINE; ENDOPEROXIDES;
Keywords:
CAROTID SINUS; PROSTACYCLIN; PLATELETS; ENDOTHELIUM; THROMBOSIS; ATHEROSCLEROSIS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
36
Recensione:
Indirizzi per estratti:
Citazione:
Z. Li et al., "ROLE OF CYCLOOXYGENASE METABOLITES IN MEDIATING PLATELET-INDUCED BARORECEPTOR DYSFUNCTION", American journal of physiology. Heart and circulatory physiology, 38(2), 1995, pp. 599-608

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 maximumbaroreceptor 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 (TxA(2)) mimetic U-46619 caused similar vasoconstriction as platelets but did not influence baroreceptor gain or maximum activity. In contrast to indomethacin, the selective TxA(2) synthesis inhibitor and receptor blocker CGS-22652 failed to influence platelet-induced suppression of activity. In summary, 1) rabbit platelets aggregating in carotid sinus suppress baroreceptor activity, which cannot be explained by the vasconstriction, and2) the suppression of activity is not mediated by TxA(2) from platelets and is opposed by prostacyclin (PGI(2)) or other prostanoids produced in carotid sinus. The combination of impaired formation of PGI(2) and platelet activation in atherosclerotic and thrombotic states may lead to profound baroreceptor dysfunction.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 13/07/20 alle ore 17:15:28