Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
INTERACTIONS BETWEEN ENDOTHELIAL SECRETAGOGUES
Autore:
GRYGLEWSKI RJ;
Indirizzi:
JAGIELLONIAN UNIV,COLL MED,DEPT PHARMACOL,16 GRZEGORZECKA PL-31531 KRAKOW POLAND
Titolo Testata:
Annals of medicine
fascicolo: 3, volume: 27, anno: 1995,
pagine: 421 - 427
SICI:
0785-3890(1995)27:3<421:IBES>2.0.ZU;2-8
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACUTE MYOCARDIAL-INFARCTION; TISSUE PLASMINOGEN-ACTIVATOR; NITRIC-OXIDE SYNTHASE; LOW-DENSITY LIPOPROTEINS; MACROPHAGE CELL-LINE; RELAXING FACTOR; L-ARGININE; PLATELET ACTIVATION; INTRAVENOUS STREPTOKINASE; THROMBOLYTIC THERAPY;
Keywords:
PROSTACYCLIN; NITRIC OXIDE; NO DONORS; TISSUE PLASMINOGEN ACTIVATOR; STREPTOKINASE; ENDOTHELIUM; THROMBOLYSIS; THROMBOGENESIS; PLATELETS; FIBRINOLYSIS; INTERACTIONS;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Science Citation Index Expanded
Citazioni:
80
Recensione:
Indirizzi per estratti:
Citazione:
R.J. Gryglewski, "INTERACTIONS BETWEEN ENDOTHELIAL SECRETAGOGUES", Annals of medicine, 27(3), 1995, pp. 421-427

Abstract

Among endothelial secretogogues prostacyclin (PGI(2)), nitric oxide (NO) and tissue plasminogen activator (t-PA) play a crucial role in maintaining thromboresistance, tone and structure of the vascular wall. Most receptor agonists, such as B-2 kinin receptor agonists, or shear force produce a coupled release of all three secretogogues, and therefore interactions between them are to be expected. Essentially, PGI(2) is a platelet suppressant, NO a vasodilator and t-PA a fibrinolytic agent. These and other properties of endothelial secretogogues supplementeach other in protecting the cardiovascular system from injuries. It is not surprising that disturbances of the secretory function of endothelial cells are associated with atherosclerosis, diabetes, thrombosisor hypertension. Traditionally, PGI(2), NO, t-PA or their substitutesare used individually for the treatment of peripheral arterial disease, angina pectoris or acute myocardial infarction. In light of recent findings, their joint administration can be advocated. For instance, NO donors will potentiate platelet-suppressant action of PGI(2) analogues, whereas exogenous PGI(2) or TXA(2) synthase inhibitors (i.e. following increase in endogenous PGI(2)) will abolish a paradox of prothrombotic action of t-PA or streptokinase. The replacement therapy with PGI(2), NO or t-PA should match as closely as possible the physiologically coupled release of these secretogogues.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 13:24:54