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E L Schiffrin - One of the best experts on this subject based on the ideXlab platform.

  • Correction of remodeling and function of small arteries in human hypertension by Cilazapril, an angiotensin I-converting enzyme inhibitor.
    Journal of cardiovascular pharmacology, 1996
    Co-Authors: E L Schiffrin
    Abstract:

    Angiotensin II may contribute to the altered structure and function of small arteries. We proposed that angiotensin I-converting enzyme (ACE) inhibitor treatment could induce a regression of vascular remodeling. A double-blind trial was performed comparing effects of the ACE inhibitor Cilazapril with the beta-blocker atenolol on small arteries obtained from biopsy specimens of subcutaneous gluteal fat. Nine patients with essential hypertension were randomized to Cilazapril and eight to atenolol. Blood pressure was below 140/95 mm Hg under treatment for the duration of the study in all patients. Media-to-lumen ratio of small arteries of the patients, which before treatment was significantly higher than in normotensive subjects, was corrected after 1 year of treatment in the Cilazapril group. There was no change in the increased media-to-lumen ratio of small arteries in the atenolol group, even after 2 years of treatment. Attenuated constrictor responses to endothelin-1 returned to normal only in the patients treated with Cilazapril. Endothelium-dependent relaxation responses to acetylcholine were slightly depressed in hypertensive patients and improved in the Cilazapril-treated group, but remained blunted in the arteries of the atenolol-treated patients. Treatment with Cilazapril corrects small artery remodeling and endothelium-related functional abnormalities of gluteal subcutaneous small arteries in hypertensive patients. It remains to be demonstrated whether these apparently beneficial effects translate into reduced morbidity and mortality in hypertension.

  • Correction of remodeling and function of small arteries in human hypertension by Cilazapril, an angiotensin I-converting enzyme inhibitor
    Journal of Cardiovascular Pharmacology, 1996
    Co-Authors: E L Schiffrin
    Abstract:

    Angiotensin II may contribute to the altered structure and function of small arteries. We proposed that angiotensin I-converting enzyme (ACE) inhibitor treatment could induce a regression of vascular remodeling. A double-blind trial was performed comparing effects of the ACE inhibitor Cilazapril with the β-blocker atenolol on small arteries obtained from biopsy specimens of subcutaneous gluteal fat. Nine patients with essential hypertension were randomized to Cilazapril and eight to atenolol. Blood pressure was below 140/95 mm Hg under treatment for the duration of the study in all patients. Media-to-lumen ratio of small arteries of the patients, which before treatment was significantly higher than in normotensive subjects, was corrected after 1 year of treatment in the Cilazapril group. There was no change in the increased media-to-lumen ratio of small arteries in the atenolol group, even after 2 years of treatment. Attenuated constrictor responses to endothelin-l returned to normal only in the patients treated with Cilazapril. Endothelium-dependent relaxation responses to acetylcholine were slightly depressed in hypertensive patients and improved in the Cilazapril-treated group, but remained blunted in the arteries of the atenolol-treated patients. Treatment with Cilazapril corrects small artery remodeling and endothelium-related functional abnormalities of gluteal subcutaneous small arteries in hypertensive patients. It remains to be demonstrated whether these apparently beneficial effects translate into reduced morbidity and mortality in hypertension.

  • remodeling of resistance arteries in human hypertension effects of Cilazapril an angiotensin i converting enzyme inhibitor
    The Cardiology, 1995
    Co-Authors: E L Schiffrin
    Abstract:

    Studies on the effect of antihypertensive agents on resistance arteries in hypertensive patients have in the past yielded inconclusive results regarding the ability of these drugs to induce a regression toward normal of either the structure or the function of these critically important vessels. We have recently compared the effects of the angiotensin-I-converting enzyme inhibitor Cilazapril and of the beta blocker atenolol on the structure and the function of subcutaneous resistance arteries of essential hypertensive patients. The patients were randomly assigned to receive either Cilazapril or atenolol for a period of 2 years. The blood pressure was normalized for the duration of the trial by both drugs. The media-to-lumen ratio of resistance arteries, which was significantly increased in all hypertensive patients before starting treatment, was normalized by the 2-year treatment with Cilazapril, whereas treatment with atenolol did not result in any change in this vascular parameter. Treatment with Cilazapril also returned to normal the contractile responses to several vasoconstrictors, particularly endothelin 1. Endothelium-dependent relaxation responses of blood vessels to acetylcholine were abnormal in hypertensive patients and improved in the Cilazapril-treated patients, but remained unchanged in the atenolol-treated ones. We conclude that treatment with the angiotensin-I-converting enzyme inhibitor Cilazapril corrects in part the vascular remodeling and the functional abnormalities of resistance arteries of hypertensive patients, whereas treatment with the beta blocker atenolol does not. These results may indicate that treatment with Cilazapril and perhaps with other angiotensin-I-converting enzyme inhibitors as well may improve the clinical outcome in hypertension by inducing a regression of abnormal resistance vessel structure and function.

Fridolin Hefti - One of the best experts on this subject based on the ideXlab platform.

  • Vascular protection with Cilazapril in hypertension.
    Journal of Cardiovascular Pharmacology, 1992
    Co-Authors: Jean-paul Clozel, Herbert Kuhn, Fridolin Hefti
    Abstract:

    Anatomical changes of arteries and arterioles secondary to hypertension explain most of the late complications of this disease. Therefore, a series of experiments was performed to characterize the vascular protective effects of Cilazapril in experimental hypertension. These experiments aimed to answer three types of questions: (a) In which vascular bed is Cilazapril effective? (b) Are the vascular changes induced by Cilazapril associated with functional effects? (c) Is the effect of Cilazapril only preventive or can Cilazapril also be effective when hypertension is already present? Our results show that Cilazapril is acting on nearly every vascular bed

  • Vascular protection with Cilazapril in hypertension.
    Journal of cardiovascular pharmacology, 1992
    Co-Authors: Jean-paul Clozel, Herbert Kuhn, Fridolin Hefti
    Abstract:

    Anatomical changes of arteries and arterioles secondary to hypertension explain most of the late complications of this disease. Therefore, a series of experiments was performed to characterize the vascular protective effects of Cilazapril in experimental hypertension. These experiments aimed to answer three types of questions: (a) In which vascular bed is Cilazapril effective? (b) Are the vascular changes induced by Cilazapril associated with functional effects? (c) Is the effect of Cilazapril only preventive or can Cilazapril also be effective when hypertension is already present? Our results show that Cilazapril is acting on nearly every vascular bed. Its vascular morphological effects (decrease of vascular hypertrophy) are associated with functional changes such as improvements of coronary or cerebral vascular reserves. Cilazapril is active either as a preventive treatment or given when hypertension is already present.

  • Vascular protection with Cilazapril.
    Drugs, 1991
    Co-Authors: Jean-paul Clozel, Herbert Kuhn, Fridolin Hefti, Jerry S. Powell, Rita K. M. Müller, Hans R. Baumgartner
    Abstract:

    The hypertrophy of the media of coronary arteries associated with hypertension reduces cross-sectional area and limits vascular reserve. Cilazapril 10 mg/kg daily decreased cardiac hypertrophy, and decreased minimal coronary vascular resistance by 40% when administered to spontaneously hypertensive rats (SHR) at the onset of hypertension. After hypertension had developed, Cilazapril restored arterial pressure to normal and increased the maximal coronary blood flow in isolated perfused hearts by 96%, which was probably a result of a marked decrease in medial hypertrophy of the coronary arteries. Similarly, Cilazapril improved cerebral vascular reserve in the mesenteric and renal arteries of SHR.

Lippincott Williams Wilkins - One of the best experts on this subject based on the ideXlab platform.

  • does the new angiotensin converting enzyme inhibitor Cilazapril prevent restenosis after percutaneous transluminal coronary angioplasty results of the mercator study a multicenter randomized double blind placebo controlled trial multicenter european
    Circulation, 1992
    Co-Authors: Lippincott Williams Wilkins
    Abstract:

    BACKGROUND Cilazapril is a novel angiotensin converting enzyme inhibitor with antiproliferative effects in the rat model after balloon injury. METHODS AND RESULTS We conducted a randomized, double-blind placebo-controlled trial to assess the effect of Cilazapril in angiographic restenosis prevention after percutaneous transluminal coronary angioplasty (PTCA). Patients received Cilazapril 2.5 mg in the evening after successful PTCA and 5 mg b.i.d. for 6 months or matched placebo. In addition, all patients received aspirin for 6 months. Coronary angiograms before PTCA, after PTCA, and at 6-month follow-up were quantitatively analyzed. In 94% of 735 recruited patients, PTCA was successful and all inclusion and exclusion criteria were met. For the per-protocol analysis, quantitative angiography after PTCA and at follow-up was available in 595 patients who complied with the treatment regimen (309 control, 286 Cilazapril). The mean difference in minimal coronary lumen diameter between post-PTCA and follow-up angiogram (primary end point) was -0.29 +/- 0.49 mm in the control group and -0.27 +/- 0.51 mm in the Cilazapril group. Clinical events during 6-month follow-up, analyzed on an intention-to-treat basis, were ranked according to the most serious clinical event ranging from death (control, two; Cilazapril, three), nonfatal myocardial infarction (control, eight; Cilazapril, 5), coronary revascularization (control, 51; Cilazapril, 53), or recurrent angina requiring medical therapy (control, 67; Cilazapril, 68) to none of the above (control, 224; Cilazapril, 212). There were no significant differences in ranking. CONCLUSIONS Long-term angiotensin converting enzyme inhibition with Cilazapril in a dose of 5 mg b.i.d. does not prevent restenosis and does not favorably influence the overall clinical outcome after PTCA.

Jean-paul Clozel - One of the best experts on this subject based on the ideXlab platform.

  • Vascular protection with Cilazapril in hypertension.
    Journal of Cardiovascular Pharmacology, 1992
    Co-Authors: Jean-paul Clozel, Herbert Kuhn, Fridolin Hefti
    Abstract:

    Anatomical changes of arteries and arterioles secondary to hypertension explain most of the late complications of this disease. Therefore, a series of experiments was performed to characterize the vascular protective effects of Cilazapril in experimental hypertension. These experiments aimed to answer three types of questions: (a) In which vascular bed is Cilazapril effective? (b) Are the vascular changes induced by Cilazapril associated with functional effects? (c) Is the effect of Cilazapril only preventive or can Cilazapril also be effective when hypertension is already present? Our results show that Cilazapril is acting on nearly every vascular bed

  • Vascular protection with Cilazapril in hypertension.
    Journal of cardiovascular pharmacology, 1992
    Co-Authors: Jean-paul Clozel, Herbert Kuhn, Fridolin Hefti
    Abstract:

    Anatomical changes of arteries and arterioles secondary to hypertension explain most of the late complications of this disease. Therefore, a series of experiments was performed to characterize the vascular protective effects of Cilazapril in experimental hypertension. These experiments aimed to answer three types of questions: (a) In which vascular bed is Cilazapril effective? (b) Are the vascular changes induced by Cilazapril associated with functional effects? (c) Is the effect of Cilazapril only preventive or can Cilazapril also be effective when hypertension is already present? Our results show that Cilazapril is acting on nearly every vascular bed. Its vascular morphological effects (decrease of vascular hypertrophy) are associated with functional changes such as improvements of coronary or cerebral vascular reserves. Cilazapril is active either as a preventive treatment or given when hypertension is already present.

  • Vascular protection with Cilazapril.
    Drugs, 1991
    Co-Authors: Jean-paul Clozel, Herbert Kuhn, Fridolin Hefti, Jerry S. Powell, Rita K. M. Müller, Hans R. Baumgartner
    Abstract:

    The hypertrophy of the media of coronary arteries associated with hypertension reduces cross-sectional area and limits vascular reserve. Cilazapril 10 mg/kg daily decreased cardiac hypertrophy, and decreased minimal coronary vascular resistance by 40% when administered to spontaneously hypertensive rats (SHR) at the onset of hypertension. After hypertension had developed, Cilazapril restored arterial pressure to normal and increased the maximal coronary blood flow in isolated perfused hearts by 96%, which was probably a result of a marked decrease in medial hypertrophy of the coronary arteries. Similarly, Cilazapril improved cerebral vascular reserve in the mesenteric and renal arteries of SHR.

Herbert Kuhn - One of the best experts on this subject based on the ideXlab platform.

  • mechanism of inhibition of neointimal formation by the angiotensin converting enzyme inhibitor Cilazapril a study in balloon catheter injured rat carotid arteries
    Arteriosclerosis Thrombosis and Vascular Biology, 1995
    Co-Authors: Jurgen Fingerle, Herbert Kuhn, Rita M K Muller, Pech Michael, Hans R. Baumgartner
    Abstract:

    Abstract We investigated the mechanism of inhibition of neointima formation by the angiotensin-converting enzyme inhibitor Cilazapril in a rat model of balloon-catheter injury in the carotid artery. We looked for the effects of Cilazapril on all phases of the response to injury, ie, on proliferation of smooth muscle cells (SMCs) in the media, their migration, their proliferation in the neointima, and their deposition of extracellular matrix in the neointima. Although treatment was discontinued after 2 weeks, the inhibitory effect of Cilazapril on neointimal formation was evident even 52 weeks after injury. The amount of extracellular matrix deposited in the intima during Cilazapril treatment was decreased by 20% 2 weeks after injury, but no effect was seen if tissues were analyzed at 4 or 52 weeks. [3H]Thymidine-labeled cells (pulse labeling as well as 14-day continuous labeling) showed a decrease in SMC labeling in the tunica media by 50%, but no inhibition in the labeling indices was seen in the neointi...

  • Vascular protection with Cilazapril in hypertension.
    Journal of Cardiovascular Pharmacology, 1992
    Co-Authors: Jean-paul Clozel, Herbert Kuhn, Fridolin Hefti
    Abstract:

    Anatomical changes of arteries and arterioles secondary to hypertension explain most of the late complications of this disease. Therefore, a series of experiments was performed to characterize the vascular protective effects of Cilazapril in experimental hypertension. These experiments aimed to answer three types of questions: (a) In which vascular bed is Cilazapril effective? (b) Are the vascular changes induced by Cilazapril associated with functional effects? (c) Is the effect of Cilazapril only preventive or can Cilazapril also be effective when hypertension is already present? Our results show that Cilazapril is acting on nearly every vascular bed

  • Vascular protection with Cilazapril in hypertension.
    Journal of cardiovascular pharmacology, 1992
    Co-Authors: Jean-paul Clozel, Herbert Kuhn, Fridolin Hefti
    Abstract:

    Anatomical changes of arteries and arterioles secondary to hypertension explain most of the late complications of this disease. Therefore, a series of experiments was performed to characterize the vascular protective effects of Cilazapril in experimental hypertension. These experiments aimed to answer three types of questions: (a) In which vascular bed is Cilazapril effective? (b) Are the vascular changes induced by Cilazapril associated with functional effects? (c) Is the effect of Cilazapril only preventive or can Cilazapril also be effective when hypertension is already present? Our results show that Cilazapril is acting on nearly every vascular bed. Its vascular morphological effects (decrease of vascular hypertrophy) are associated with functional changes such as improvements of coronary or cerebral vascular reserves. Cilazapril is active either as a preventive treatment or given when hypertension is already present.

  • Vascular protection with Cilazapril.
    Drugs, 1991
    Co-Authors: Jean-paul Clozel, Herbert Kuhn, Fridolin Hefti, Jerry S. Powell, Rita K. M. Müller, Hans R. Baumgartner
    Abstract:

    The hypertrophy of the media of coronary arteries associated with hypertension reduces cross-sectional area and limits vascular reserve. Cilazapril 10 mg/kg daily decreased cardiac hypertrophy, and decreased minimal coronary vascular resistance by 40% when administered to spontaneously hypertensive rats (SHR) at the onset of hypertension. After hypertension had developed, Cilazapril restored arterial pressure to normal and increased the maximal coronary blood flow in isolated perfused hearts by 96%, which was probably a result of a marked decrease in medial hypertrophy of the coronary arteries. Similarly, Cilazapril improved cerebral vascular reserve in the mesenteric and renal arteries of SHR.