Search results for "Losartan"

Effects of Losartan and Delapril on the Fibrinolytic System in Patients with Mild to Moderate Hypertension

2007

Background and objectives: Angiotensin-converting enzyme (ACE) probably influences the fibrinolytic system at a central point by converting angiotensin I to angiotensin II, which increases plasminogen activator inhibitor-1 (PAI-1) activity. This effect appears to be mediated in humans via the angiotensin II type 1 (AT1) receptor. The objective of this study was to evaluate, in patients with mild to moderate hypertension, the change in tissue plasminogen activator (t-PA) and PAI-1 plasma levels after treatment with an AT1-receptor blocker (losartan 50 mg/day) or an ACE inhibitor (delapril 60 mg/day). Patients and methods: 30 hypertensive patients and 15 controls were enrolled. Essential hype…

Different effects of losartan and delapril on plasma PAI-1 levels in patients with mild to moderate hypertension

2003

ACE probably influences the fibrinolytic system at acentral point by converting angiotensin I to angiotensin II,which increases PAI-1 activity. This effect appears to bemediated via the AT1-receptor in humans. The RAAS mayalso contribute to a reduction in t-PA production by degra-dation of bradykinin, since the latter increases the release ofprostacyclin, nitric oxide, and t-PA from endothelial cells.Accordingly, ACE inhibitors not only influence the fibrino-lytic system by a reduction of PAI-1 activity but also byincreasing t-PA activity [1–3]. However, few studies haveanalysed the effects of AT1-R antagonists on t-PA and PAI-1plasma levels and the in vivo effects of AT1-R antagonistson th…

Experimental Study of the Effects of EIPA, Losartan, and BQ-123 on Electrophysiological Changes Induced by Myocardial Stretch

2015

[ES] Introducción y objetivos Se han implicado diversos mecanismos en la respuesta mecánica al estiramiento miocárdico, que incluyen la activación del intercambiador Na+/H+ por acciones autocrinas y paracrinas. Se estudia la participación de estos mecanismos en las respuestas electrofisiológicas al estiramiento agudo miocárdico mediante el análisis de los cambios inducidos con fármacos. Métodos Se analizan las modificaciones de la fibrilación ventricular inducidas por el estiramiento agudo miocárdico en corazones de conejo aislados y perfundidos utilizando electrodos múltiples epicárdicos y técnicas cartográficas. Se estudian 4 series: control (n = 9); durante la perfusión del antagonista d…

The loss of muscle mass and sarcopenia: non hormonal intervention.

2011

Muscle aging is a key component of the increase in frailty in human populations. The generation of critical levels of power is a prerequisite to perform simple tasks of daily living, such as rising from a chair or climbing stairs. There is great scientific and social interest to determine which behaviors can lead to the maintenance of the muscle mass in young immobilized subjects and in the elderly. Several hormonal treatments have been proposed for the treatment of sarcopenia. However, the side effects associated to these treatments emphasize the need of finding non-toxic and non-hormonal treatments that help increase muscle strength, improve muscle function, and decrease the degree of dep…

Irbesartan results in more complete blockade of human renal at1-receptor mediated effects than does candesartan cilexetil as evidenced by higher plas…

2000

Inhibition of sympathetic activity induced by losartan in essential hypertensives.

1999

L-NAME induces direct arteriolar leukocyte adhesion, which is mainly mediated by angiotensin-II.

2005

Acute inhibition (1 h) of nitric oxide synthase (NOS) with L-NAME causes leukocyte recruitment in the rat mesenteric postcapillary venules that is angiotensin-II (Ang-II) dependent. Since 4-h exposure to Ang-II provokes arteriolar leukocyte adhesion, this study was designed to investigate whether subacute (4-h) NOS inhibition also causes this effect.Rats were intraperitoneally injected with saline, L-NAME, or 1H-[1,2,4]-oxidazolol-[4,3-a]-quinoxalin-1-one (ODQ). Leukocyte accumulation in the mesenteric microcirculation was examined 4 h later via intravital microscopy. Some groups were pretreated with losartan, an AT(1) Ang-II receptor antagonist.At 4-h, L-NAME caused a significant increase …

Arterial and Venous Endothelia Display Differential Functional Fractalkine (CX 3 CL1) Expression by Angiotensin-II

2012

Objective— Angiotensin-II (Ang-II) promotes the interaction of mononuclear cells with arterioles and neutrophils with postcapillary venules. To investigate the mechanisms underlying this dissimilar response, the involvement of fractalkine (CX 3 CL1) was explored. Methods and Results— Enhanced CX 3 CL1 expression was detected in both cremasteric arterioles and postcapillary venules 24 hours after Ang-II intrascrotal injection. Arteriolar leukocyte adhesion was the unique parameter significantly reduced (83%) in animals lacking CX 3 CL1 receptor (CX 3 CR1). Human umbilical arterial and venous endothelial cell stimulation with 1 μmol/L Ang-II increased CX 3 CL1 expression, yet neutralization …

Transforming growth factor β1 and additional renoprotective effect of combination ACE inhibitor and angiotensin II receptor blocker in hypertensive s…

2005

Objective To verify the benefit of renin–angiotensin system blockade in hypertension, the effects of 24 weeks’ losartan and ramipril treatment, both alone and in combination, on urinary albumin excretion (UAE) and circulating transforming growth factor b1 (TGFb1) have been evaluated in hypertensive subjects with minor renal abnormalities. Design and methods Fifty-one patients with stage 1 and 2 essential hypertension and with UAE >—20 mg/24 h but with maintained renal function have been included. After a 4-week run-in with placebo administration, a randomized double-blind, three-arm double-dummy trial was used. All the hypertensives (HT) were allocated randomly to three treatment arms (1…

Estrogens inhibit angiotensin II-induced leukocyte-endothelial cell interactions in vivo via rapid endothelial nitric oxide synthase and cyclooxygena…

2002

Angiotensin II (Ang II) may be a key molecule in the development of atherosclerosis. Because the incidence of coronary atherosclerosis in premenopausal women is lower than that observed in men or postmenopausal women, we have investigated the effect of estrogens on Ang II–induced leukocyte recruitment in vivo using intravital microscopy in the rat mesenteric microcirculation. Superfusion for 60 minutes with Ang II induced a significant increase in leukocyte rolling flux, adhesion, and emigration. Administration of 17-β-estradiol (17-β-E) after 30 minutes of Ang II superfusion produced a reduction of these leukocyte responses by 55.1%, 72.7%, and 70.9%, respectively, an additional 30 minutes…