Angiotensin Receptor

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Hayo Castrop - One of the best experts on this subject based on the ideXlab platform.

  • Angiotensin Receptor-associated proteins: local modulators of the renin–Angiotensin system
    Pflügers Archiv - European Journal of Physiology, 2013
    Co-Authors: Hayo Castrop
    Abstract:

    The activity of the reninAngiotensin system crucially depends on the rate of renal renin secretion. Changes in renin secretion result in fluctuations of Angiotensin II concentrations in the circulation and subsequently in the activation of Angiotensin Receptors in all accessible target organs. Consequently, various mechanisms have evolved to regulate the local sensitivity to Angiotensin II. In this review, an overview of Angiotensin II Receptor-associated proteins is addressed. These proteins regulate the local sensitivity of Receptor-expressing cells by modulating the Receptor surface expression and the Receptor sensitivity. A hypothesis will be discussed that integrates the existence of various Angiotensin Receptor-associated proteins into an overall functional model.

  • Angiotensin Receptor-associated proteins: local modulators of the renin-Angiotensin system.
    Pflugers Archiv : European journal of physiology, 2012
    Co-Authors: Hayo Castrop
    Abstract:

    The activity of the reninAngiotensin system crucially depends on the rate of renal renin secretion. Changes in renin secretion result in fluctuations of Angiotensin II concentrations in the circulation and subsequently in the activation of Angiotensin Receptors in all accessible target organs. Consequently, various mechanisms have evolved to regulate the local sensitivity to Angiotensin II. In this review, an overview of Angiotensin II Receptor-associated proteins is addressed. These proteins regulate the local sensitivity of Receptor-expressing cells by modulating the Receptor surface expression and the Receptor sensitivity. A hypothesis will be discussed that integrates the existence of various Angiotensin Receptor-associated proteins into an overall functional model.

Stefan Peters - One of the best experts on this subject based on the ideXlab platform.

  • Can Angiotensin Receptor Antagonists Prevent Restenosis After Stent Placement?
    American Journal of Cardiovascular Drugs, 2002
    Co-Authors: Stefan Peters
    Abstract:

    Restenosis rates after coronary stent implantation in complex lesions are between 30 and 50%. Neointimal hyperplasia promoted by complex interaction between cellular and acellular elements, such as cytokines and growth factors, is thought to be the primary process responsible for restenosis. The risk of in-stent restenosis is increased in patients with a history of restenosis after percutaneous transluminal coronary angioplasty, in long lesions, in total occlusions, in patients with diabetes mellitus, in small vessels, in the proximal parts of the left anterior descending coronary artery and in cases of stent oversizing. In-stent restenosis represents a serious economic burden on society because treatment strategies include expensive approaches such as cutting-balloon angioplasty, rotational atherectomy and brachytherapy. A number of pharmacological agents, including ACE inhibitors, have been unsuccessful in preventing restenosis. Alternative procedures such as brachytherapy, radioactive stents and drug-eluting stents are under evaluation. Although sirolimus- or paclitaxel-eluting stents have been associated with very low restenosis rates over durations of 6 to 12 months, the long-term efficacy and tolerability of this approach is currently being investigated. Although ACE inhibitors have failed in reducing restenosis rates, the selective Angiotensin II type 1 (AT_1) Receptor antagonist valsartan has shown encouraging results in the single-center Valsartan for Prevention of Restenosis after Stenting of Type B2/C lesions trial (ValPREST). The ValPREST trial is the first randomized, placebo-controlled study to have evaluated the effect of an Angiotensin Receptor antagonist on in-stent restenosis in a moderate number of patients. Compared with ACE inhibitors, Angiotensin Receptor blockers exert additional effects on the pathophysiological processes which lead to restenosis. Angiotensin Receptor antagonists may affect several mechanisms involved in neointimal hyperplasia such as decreasing circulating cytokine and growth factor levels and reducing neutrophil activation, especially after stenting in acute coronary syndromes, but the results need to be confirmed in a large multicenter trial. The question whether long-term therapy, with an oral Angiotensin Receptor antagonist, is cost-effective and whether Angiotensin Receptor antagonists should be used as an add-on therapy to drug-eluting stents, requires clarification.

  • Can Angiotensin Receptor Antagonists Prevent Restenosis After Stent Placement?
    American Journal of Cardiovascular Drugs, 2002
    Co-Authors: Stefan Peters
    Abstract:

    Restenosis rates after coronary stent implantation in complex lesions are between 30 and 50%. Neointimal hyperplasia promoted by complex interaction between cellular and acellular elements, such as cytokines and growth factors, is thought to be the primary process responsible for restenosis. The risk of in-stent restenosis is increased in patients with a history of restenosis after percutaneous transluminal coronary angioplasty, in long lesions, in total occlusions, in patients with diabetes mellitus, in small vessels, in the proximal parts of the left anterior descending coronary artery and in cases of stent oversizing. In-stent restenosis represents a serious economic burden on society because treatment strategies include expensive approaches such as cutting-balloon angioplasty, rotational atherectomy and brachytherapy. A number of pharmacological agents, including ACE inhibitors, have been unsuccessful in preventing restenosis. Alternative procedures such as brachytherapy, radioactive stents and drug-eluting stents are under evaluation. Although sirolimus- or paclitaxel-eluting stents have been associated with very low restenosis rates over durations of 6 to 12 months, the long-term efficacy and tolerability of this approach is currently being investigated. Although ACE inhibitors have failed in reducing restenosis rates, the selective Angiotensin II type 1 (AT_1) Receptor antagonist valsartan has shown encouraging results in the single-center Valsartan for Prevention of Restenosis after Stenting of Type B2/C lesions trial (ValPREST). The ValPREST trial is the first randomized, placebo-controlled study to have evaluated the effect of an Angiotensin Receptor antagonist on in-stent restenosis in a moderate number of patients. Compared with ACE inhibitors, Angiotensin Receptor blockers exert additional effects on the pathophysiological processes which lead to restenosis. Angiotensin Receptor antagonists may affect several mechanisms involved in neointimal hyperplasia such as decreasing circulating cytokine and growth factor levels and reducing neutrophil activation, especially after stenting in acute coronary syndromes, but the results need to be confirmed in a large multicenter trial. The question whether long-term therapy, with an oral Angiotensin Receptor antagonist, is cost-effective and whether Angiotensin Receptor antagonists should be used as an add-on therapy to drug-eluting stents, requires clarification.

A Desai - One of the best experts on this subject based on the ideXlab platform.

  • Current status of Angiotensin Receptor blockers for the treatment of cardiovascular diseases: focus on telmisartan
    Journal of Human Hypertension, 2005
    Co-Authors: S G Chrysant, G S Chrysant, A Desai
    Abstract:

    Poorly controlled hypertension is a major risk for cardiovascular morbidity and mortality, strokes, heart failure and renal failure. Despite these devastating complications, blood pressure control of ⩽140/90 mmHg, which is above the current standard, is very poor worldwide, accounting for 34% of hypertensive patients in the United States, and 6% in other countries. The reasons for this poor control of blood pressure include lack of aggressive treatment by physicians, especially for the systolic blood pressure, drug selection and patient compliance. The blood pressure follows a circadian rhythm and is the highest between 0600 to 1200 h, when most complications occur. Long-acting drugs that extend their action to cover this vulnerable period are preferable, especially those that block the reninAngiotensin–aldosterone system, such as ACE inhibitors and Angiotensin Receptor blockers, and are the most effective in controlling blood pressure and preventing or reducing its cardiovascular and renal complications. With respect to the Angiotensin Receptor blockers, telmisartan has been demonstrated by several studies to be the longest acting among its class of drugs and to effectively prevent the early morning rise of blood pressure.

  • Current status of Angiotensin Receptor blockers for the treatment of cardiovascular diseases: focus on telmisartan
    Journal of human hypertension, 2005
    Co-Authors: S G Chrysant, G S Chrysant, A Desai
    Abstract:

    Current status of Angiotensin Receptor blockers for the treatment of cardiovascular diseases: focus on telmisartan

Dg Beevers - One of the best experts on this subject based on the ideXlab platform.

Andrew P Ambrosy - One of the best experts on this subject based on the ideXlab platform.

  • the role of Angiotensin Receptor neprilysin inhibitors in cardiovascular disease existing evidence knowledge gaps and future directions
    European Journal of Heart Failure, 2018
    Co-Authors: Andrew P Ambrosy, Robert J Mentz, Mona Fiuzat, John G F Cleland, Stephen J Greene, Christopher M Oconnor
    Abstract:

    Although traditional renin-Angiotensin system antagonists including Angiotensin-converting enzyme inhibitors and Angiotensin Receptor blockers have revolutionized the treatment of cardiovascular disease (CVD), the pivotal PARADIGM-HF trial demonstrated that sacubitril/valsartan, an Angiotensin Receptor-neprilysin inhibitor (ARNI), was superior to an Angiotensin-converting enzyme inhibitor in reducing cardiovascular morbidity and mortality in patients with heart failure and reduced ejection fraction. However, despite international regulatory approval and strong recommendations in the guidelines, uptake of sacubitril/valsartan has been disappointing. Sacubitril/valsartan is now the focus of a large programme of clinical trials testing the hypothesis that ARNIs may supplant conventional renin-Angiotensin system inhibitors across the spectrum of CVD, including hypertension, secondary prevention after myocardial infarction, and heart failure with preserved ejection fraction. This review summarizes the existing evidence, knowledge gaps, and future directions of ARNIs in CVD based on discussions between clinical trialists, industry representatives, and regulatory authorities at the 2016 Global CardioVascular Clinical Trialists Forum in Washington, D.C.