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Titolo:
Fibrinolytic function in diuretic-induced volume depletion
Autore:
Lottermoser, K; Hertfelder, HJ; Vetter, H; Dusing, R;
Indirizzi:
Univ Bonn, Med Poliklin, D-53111 Bonn, Germany Univ Bonn Bonn Germany D-53111 Bonn, Med Poliklin, D-53111 Bonn, Germany Inst Expt Hamatol & Transfus Med, Bonn, Germany Inst Expt Hamatol & Transfus Med Bonn Germany ansfus Med, Bonn, Germany
Titolo Testata:
AMERICAN JOURNAL OF HYPERTENSION
fascicolo: 4, volume: 13, anno: 2000,
parte:, 1
pagine: 359 - 363
SICI:
0895-7061(200004)13:4<359:FFIDVD>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLASMINOGEN-ACTIVATOR INHIBITOR; RENIN-ANGIOTENSIN SYSTEM; CONVERTING ENZYME GENE; ISCHEMIC-HEART-DISEASE; MYOCARDIAL-INFARCTION; ESSENTIAL-HYPERTENSION; ENDOTHELIAL-CELLS; RISK FACTOR; PLASMA; EXPRESSION;
Keywords:
angiotensin II; diuretics; hydrochlorothiazide; plasma renin activity; plasminogen activator inhibitor 1; tissue plasminogen activator;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Dusing, R Univ Bonn, Med Poliklin, Wilhelmstr 35-37, D-53111 Bonn, GermanyUniv Bonn Wilhelmstr 35-37 Bonn Germany D-53111 1 Bonn, Germany
Citazione:
K. Lottermoser et al., "Fibrinolytic function in diuretic-induced volume depletion", AM J HYPERT, 13(4), 2000, pp. 359-363

Abstract

Accumulating evidence suggests that the renin-angiotensin system (RAS) mayparticipate in the regulation of fibrinolytic function. In clinical studies, however, angiotensin-converting enzyme (ACE) inhibitors and the angiotensin II receptor antagonist losartan have failed to consistently affect endogenous fibrinolysis. Because such an effect may depend on the degree of prestimulation of the RAS, we have studied parameters of fibrinolytic functionin 15 healthy volunteer subjects during baseline (day 1) and after 10 daysof treatment with 25 mg of hydrochlorothiazide (HCT)/day (day 11). On the last day of the study (day 12), a single oral dose of 50 mg of losartan wasgiven to the volunteers in addition to HCT and fibrinolytic function was assessed at the peak effect of losartan (5 h later). Plasma renin activity (PRA) was significantly stimulated during diuretic treatment (1.35 +/- 0.21 v 0.34 +/- 0.06 ng mL(-1).h(-1) [P < .001]) and further increased after losartan (6.39 +/- 1.16 ng mL(-1).h(-1) [P < .001]). No effects of either the diuretic or losartan could be observed on tissue-type plasminogen activator(t-PA) antigen concentration and activity. However, 10 days of treatment with HCT significantly increased plasminogen activator inhibitor-1 (PAI-1) antigen (26.8 +/- 5.8 v 21.1 +/- 3.4 ng/mL [p =.037]). In addition, PAI-1 activity was also tentatively raised by HCT treatment (5.48 +/- 1.82 v 3.88 +/- 0.79 IU/mL [P = .067]). In spite of the marked further rise in PRA afterlosartan, the stimulation of PAI-1 antigen and activity was blunted by losartan (24.4 +/- 3.6 ng/mL and 4.55 +/- 0.99 IU/mL, respectively). Our results demonstrate that volume depletion induced by HCT treatment is associatedwith a rise in PAI-1. Acute administration of losartan is capable of blunting this effect, suggesting that the angiotensin II type 1 receptor may participate in this effect of angiotensin II. (C) 2000 American Journal of Hypertension, Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 15:49:50