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 13,001 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The renin angiotensin system is implicated in the development of vein graft disease after coronary artery bypass surgery. Components of this system have been shown to play important roles in determining the short-term and long-term performance of coronary artery bypass grafts. Significant differences exist in the commonly used arterial and venous grafts in angiotensin converting enzyme activity and angiotensin responses. The existence of a dual enzyme pathway in angiotensin II formation has also been demonstrated. Such findings have implications for the use of AT1-receptor antagonists over enzyme inhibitors to improve graft performance and prevent the development of coronary artery bypass graft disease.
Curr Opin Cardiol 2000 Nov
PMID:The renin angiotensin system in bypass graft surgery. 1119 18

Mechanical forces have profound effects on cardiomyocytes. To test whether angiotensin II is a potential mediator of stretch-induced effects on gap junctions, we used the angiotensin II (AT1) receptor antagonist, losartan, to investigate the cyclical stretch-induced expression of connexin43 (Cx43), the major cardiac muscle gap junction channel protein. Cultured neonatal rat cardiomyocytes grown on a flexible membrane base were stretched by vacuum to 20% of maximum elongation, at 60 cycles/min. The levels of Cx43 protein began to increase as early as 2 h after stretch was applied, reached a maximum of six-fold over the control by 24 h and remained at this level another 24 h (i.e. up to 48 h after stretch was applied). These increases of Cx43 protein at 24 h were largely (73%) and completely (100%) attenuated (P<0.001) by the addition (30 min before stretch) of 10 n M and 100 n M losartan, respectively. Similarly, the Cx43 mRNA levels in stretched cardiomyocytes rose 89% (P<0.01) above control (non-stretched cells) mRNA levels. This increase also was blocked by losartan. Cyclical stretch increased (and losartan decreased) the immunohistochemical labeling of Cx43 and significantly increased release of angiotensin II into the culture media from 7.5+/-0.6 ng/ml to 23.8+/-1.0 ng/ml (P<0.01) after a 1 h stretch. These findings indicate that cyclical mechanical stretch augments angiotensin II production and Cx43 gene expression in cultured cardiomyocytes, partially through mediation of the AT1 receptors, and suggests interaction between the cardiomyocyte local rennin-angiotensin system and Cx43 in response to stretch.
J Mol Cell Cardiol 2001 Apr
PMID:Angiotensin II receptor antagonist blocks the expression of connexin43 induced by cyclical mechanical stretch in cultured neonatal rat cardiac myocytes. 1127 22

The development of pharmacological agents that block the renin-angiotensin system (RAS) specifically have helped to define all the components of the system and their contribution to blood-pressure control and to the pathogenesis of hypertension, congestive heart failure and chronic renal failure. The angiotensin converting-enzyme inhibitors (ACEi) are among all available drugs that interfere with the RAS, the most efficient, so far, in the treatment of several cardiovascular diseases, with comfortable posologic schemes and an acceptable safety profile. The most important difference between them are more related to pharmacokinetic profile rather than to pharmacodynamic characteristics. With the use of ACEi the interference with other neurohumoral systems is unavoidable and the controversy has been pharmacologically and clinically installed. With the advent of oral selective AT1 angiotensin II receptor blockers (ARB) the pharmacological interference became eventually much more selective. Their antihypertensive efficacy is identical and their tolerability is better than that showed by ACEi. The ARBs differ mainly in their pharmacokinetics and in their binding capacity to the AT1 angiotensin receptor. The results of several ongoing clinical trials will show if the ARBs as ACEi will be capable to protect target-organs and to promote a significant reduction in cardiovascular morbility and mortality. In parallel there is an intense experimental and clinical research with other groups of drugs which also markedly interfere with RAS: renin inhibitors, chymase inhibitors and simultaneous inhibitors of vasopeptidases (ACE, endothelin converting-enzyme, neutral endopeptidase). From the pharmacological point of view, it is now possible to block effectively RAS with some relevant clinical results that will be certainly widen in the near future.
Rev Port Cardiol 2000 Dec
PMID:[Angiotensin converting enzyme inhibitors (ACEIs) and angiotensin II receptor antagonists. Pharmacologic features]. 1130 8

The A II antagonists (RA II antagonists) are a new group of anti-hypertensive drugs with five years of clinical use. They were investigated after the knowledge of independent ways to get angiotensin II. They block AT1 receptor. It's possible that, after AT1 block, the high plasmatic levels of AII stimulate the AT2 receptors with vasodilation and anti-proliferative activity. We are waiting for the results of several big prospective studies with RA II antagonists on cardiovascular morbidity and mortality. At present time, the first indication for its use is the appearance of cough when taking ACE inhibitors. The association of ACE inhibitors and RA II antagonists can improve some clinical conditions like dilated hypertensive cardiopathy, nephropathy or refractory hypertension.
Rev Port Cardiol 2000 Dec
PMID:[ACE inhibitors versus AR II antagonists. Their role in arterial hypertension]. 1130 10

After recalling the fundamental importance of ACE inhibitors in the treatment of heart failure, the author analyzes the scientific evidence supporting the use of beta-adrenergic blockers in the treatment of this syndrome. He describes the complications involved in prescribing these drugs for patients in functional class IV and reviews the current literature on the problem. He then considers the possibility of beta-blockers (particularly carvedilol) being used instead of ACE inhibitors. He reviews the conclusions of studies on the benefits of adding an AT1 receptor antagonist to ACE inhibitor therapy, including the results of the RESOLVD studies. He also concludes that there is no evidence that AT2 receptor antagonists are as good as or better than ACE inhibitors in the treatment of heart failure.
Rev Port Cardiol 2001 Mar
PMID:[Options in drug combinations]. 1140 73

The arrival of angiotensin converting enzyme inhibitors (ACE), and AT1 angiotensin selective receptors blockers, has changed the panorama of systemic high blood pressure and cardiac insufficiency treatments. These inhibitors and blockers have also been useful in cases of left asymptomatic ventricular dysfunction, myocardial infarction and post-infarction and various nephropathies--not only diabetes dependent but due to other etiologies as well. Furthermore, its application in primary prevention of coronary cardiopathies has started to become evident. The main advantages of this new group of drugs are their relative harmlessness and lesser undesirable side effects, as those caused by other antihypertensives agents. The AT1 receptor inhibitors of angiotensin have actually not proven to be superior than the ACE inhibitors (although the latter are not worse) but are better tolerated and protect a greater period of time with a single dosage. A greater number of macro studies with selective AT1 receptor blockers is necessary to know its right place in therapeutics.
Arch Cardiol Mex
PMID:[Converting enzyme inhibitors or AT1 receptor blockers]. 1156 29

Studies performed in the last five years have led to the knowledge of new mechanisms by which the hypertensive process produces hypertrophy and cardiac fibrosis, at the same time, favoring development of the atheroesclerotic plaque. The Renin-Angiotensin-Aldosterone axis is relevant by involved in the physiopathology of these alterations, not only by producing hyperplasia and hypertrophy of vascular smooth muscle cells or by increasing protein and DNA syntheses, mediated by Angiotensin II (by itself a potent Growth factor) but also through inflammatory processes exerted upon the vascular smooth muscle cells. These alterations (hypertrophy, fibrosis, inflammation, and destabilization of the atherosclerotic plaque) can now be counteracted by blocking the Angiotensin-Converting enzyme or its AT1 receptors with the consequent improvement in ventricular diastolic functions.
Arch Cardiol Mex
PMID:[The heart in hypertension. Cardiac protection and cardiac repair]. 1200 49

Essential hypertension, a major health problem worldwide, is a disease generally considered to require life-long treatment. However, evidence suggests that hypertension is caused by specific phenotypic changes caused by the combination of genetic and environmental factors. Thus, in principle, hypertension could be prevented by prevention of these phenotypic changes. Animal data indicate that early treatment that blocks the renin-angiotensin system have long-term effects after treatment withdrawal. Here we report on two human trials that are testing whether early treatment (with the AT1-antagonist, candesartan) is able to have a persistent effect after stopping treatment: the Danish Hypertension Prevention Project and Trial of Prevention of Hypertension.
Curr Opin Cardiol 2002 Jul
PMID:Can hypertension be prevented? The Danish Hypertension Prevention Project and the Trial of Prevention of Hypertension studies. 1215 73

Valsartan, an angiotensin II antagonist with a potent and highly selective effect on AT1 receptors, has been found effective and safe in several randomized, controlled studies versus a placebo, other antihypertensive agents, or other angiotensin II antagonists. An eight-week, open-label, multicenter, prospective, pragmatic, phase IV trial was conducted by office-based cardiologists to evaluate the clinical safety and efficacy of valsartan 80 mg in everyday practice. The efficacy analysis included 3084 patients given valsartan alone for four weeks then, during the next four weeks, either valsartan alone or, if the diastolic blood pressure was still > or = 90 mmHg, valsartan in combination with another antihypertensive agent. The valsartan dosage was 80 mg/day. On day 28, 64% of patients were controlled and 78% were responders. The safety analysis included 3,108 patients. Of the 239 medical adverse events ascribed by the investigators to the study treatment, 72 led to premature study discontinuation. This figure translated into a 2.68% rate among treated patients, which is similar to the 2.3% rate recorded during the placebo-controlled trials performed as part of the valsartan clinical development program. These results confirm the outstanding safety profile of valsartan.
Ann Cardiol Angeiol (Paris) 2000 Feb
PMID:[Tolerance to valsartan in office practice in 3,197 hypertensive patients (the VALSE study)]. 1255 16

Because it is uncertain whether high-pressure stent deployment may contribute to more exuberant neointimal proliferation, a new stent, the LP , was constructed to allow full expansion at 10 atmospheres (atm). We compared in a randomized trial the 6-month target vessel revascularization (TVR) and other clinical outcomes of the LP stent with the most commonly used Food and Drug Administration-approved stent (Guidant Duett and Tristar stents) in 1,003 patients without a recent myocardial infarction. The first 150 patients assigned the LP stent also underwent repeat angiography at 6 months. Baseline characteristics for the two groups were balanced, except for an excess of unstable angina in the LP group. There was slight excess in failure to deliver the LP stent (3.4% versus 1.4%; p = 0.04), and similar 7-day rates of procedural success without ischemic complications (92% versus 93%; p = 0.53). More patients in the LP group had pre-dilation (72% versus 58%; p < 0.001) and post-dilatation (61% versus 50%; p = 0.001). The stent deployment pressure was significantly lower, as expected, in the LP group (10 2 ATM versus 13 4 atm; p < 0.001). At 30 days, the incidence of major adverse cardiac events was similar. At 6 months, the incidence of TVR was 10% and 7.8%, respectively (p = 0.28), hazard ratio was 0.79 (0.52 1.21), and absolute difference was 2.2% (-2.3% to 6.7%), well within the range of equivalency set at 7.5%. Patients without post-dilatation had a significantly higher rate of revascularization with the LP stent than with the Guidant stent (p = 0.02). Thus, the new LP stent achieves rates of revascularization that are not inferior to the Guidant stent, but this effect cannot be linked to lower-pressure deployment.
J Invasive Cardiol 2003 Mar
PMID:A randomized multicenter trial comparing a new, low-pressure versus a conventional coronary stent: primary results from the CONSERVE trial. 1261 86


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