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The studied cohort consisted of 11 patients with CGN, hypertension and proteinuria > 400 mg/24 h. Four drugs were given for 4 weeks, doubly blinded and randomized according to a "Latin-square design": Celiprolol (beta-1-antagonist, beta-2-agonist, 200 mg/d), Atenolol (selective beta-1-antagonist, 50 mg/d), Ramipril (ACE-inhibitor, 2.5 mg/d) and placebo. There was a two-week wash-out phase between each of the four treatment phases. At the end of each treatment phase glomerular filtration rate (GFR) and effective renal plasma flow (ERPF) were measured by inulin and para-amino-hippuric acid (PAH) clearance. Proteinuria was determined in the course of a three-day collection period at the end of each treatment phase. During this period blood pressures were measured with a continuous 24-hour blood pressure monitor.
Chronic ACE inhibition increases anti-fibrotic BK and does not attenuate LV remodeling in pure VO. The relative contribution of changes in extracellular matrix versus cardiomyocyte elongation in acute and chronic LV chamber remodeling during VO is unknown.
Pulverized atenolol, bisoprolol, enalapril and ramipril are poor tasting. From the perspective of palatability, pulverized chlorthalidone, hydrochlorothiazide and lisinopril are preferable.
We have previously shown that transplantation of kidneys from genetically hypertensive to normotensive rats result in hypertension in renal graft recipients. To investigate whether this posttransplantation hypertension may have been the result of damage to the renal graft by high perfusion pressure before transplantation, we normalized blood pressure throughout life in spontaneously hypertensive rat (SHR) kidney donors by continuous antihypertensive treatment with the angiotensin-converting enzyme inhibitor ramipril (1 mg.kg-1.day-1 in drinking fluid). When kidneys from these rats were transplanted at age 20 wk to age-matched bilaterally nephrectomized F1 hybrids bred from SHR and Wistar-Kyoto (WKY) parents, posttransplantation hypertension still developed. In contrast, blood pressure did not change significantly in recipients of kidneys from ramipril-treated WKY rats. In the initial phase, recipients of SHR kidneys had a lower body weight and higher plasma urea concentrations than recipients of WKY kidneys. However, in the chronic phase, there were no significant differences between the two groups with respect to daily water intake, plasma urea concentration, glomerular filtration rate, renal blood flow, and weight of transplanted kidneys; no histological differences were observed between renal grafts from WKY and SHR donors, except for structural vascular hypertrophy in the latter group. We conclude that posttransplantation hypertension in recipients of SHR kidney grafts also develops, when the grafts have not been subjected to high renal perfusion pressure before transplantation. Our data support the hypothesis that SHR kidneys carry a primary defect, which can induce hypertension in renal graft recipients.
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Twenty-nine patients with LV ejection fraction <40% received the ACE inhibitor ramipril (range 2.5 to 20 mg/day) within 5 days of their first Q-wave MI. Magnetic resonance imaging was performed at baseline and at 3 months, providing global and regional LV volumes and mass from summated serial short-axis slices. Mean arterial blood pressure was unchanged from baseline to 3-month follow-up (89 +/- 10 to 92 +/- 17 mm Hg). LV mass decreased (90 +/- 25 to 77 +/- 21 gm/m2, p < 0.0005) as LV end-diastolic volumes increased (65 +/- 13 to 73 +/- 22 ml/m2, p < 0.01). Global LV mass to volume ratio decreased from 1.40 +/- 0.28 to 1.08 +/- 0.18 gm/ml (p < 0.0001), as did circumferential wall thickness to volume ratio of noninfarcted myocardium at the base of the LV (0.06 +/- 0.02 to 0.05 +/- 0.02 mm/ml, p < 0.001). LV ejection fraction increased from 35 +/- 6 to 40 +/- 9% (p < 0.001) in the presence of an increase in calculated end-systolic wall stress (185 +/- 57 to 227 +/- 54 gm/cm2, p < 0.01).
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In placebo-treated MI rats, six weeks after MI, left ventricular circumference, inner diameter, and left ventricular end-diastolic pressure (LVEDP) were increased, whereas mean arterial blood pressure (MAP) and maximum rate of rise of left ventricular pressure (dp/dt(max)) were decreased compared with sham-operated controls (P<0.01). In ramipril-treated MI rats, heart weight, heart weight to body weight ratio and interstitial collagen content were reduced (P<0.05, P<0.01), LVEDP was slightly decreased (P>0.05), and dp/dt(max) was improved (P<0.01) compared with placebo-treated MI rats. In contrast, in mibefradil-treated MI rats, heart weight, heart weight to body weight ratio were slightly but not significantly reduced, LVEDP was slightly elevated compared with placebo-treated MI rats, and was elevated (P<0.05) compared with ramipril-treated MI rats, although interstitial collagen content were reduced (P<0.01) compared with placebo-treated MI rats.
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Thirty-five 5-week-old rats were included in the study: six TGRs received RAM; five TGRs RAM + the bradykinin receptor inhibitor, icatibant; six TGRs, MDL; and five TGRs MDL + icatibant, while eight TGRs and five normotensive Sprague-Dawley controls were kept untreated. Mesenteric small arteries were dissected and mounted on a micromyograph. The media-to-lumen ratio (M/L) was then calculated. Vascular metalloproteinase (MMP) content was evaluated by zymography.
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As component of PGDFM course, this study was conducted to provide better understanding of prevalent ailments and common treatment provided by the GPs in the community at present giving key insight of current practice in rural area by a registered family medicine practitioner.
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We estimated the cost effectiveness of adding the ACE inhibitor ramipril to conventional treatment in patients with heart failure after acute myocardial infarction. These estimates were based on the Acute Infarction Ramipril Efficacy (AIRE) study and on complementary Swedish healthcare resource use data for a subset of patients. The average follow-up period was 15 months (minimum 6 months, maximum 3.8 years). The perspective of the analysis was that of the county councils (third-party payers), and we focused on the cost of drugs and hospitalisation. The marginal cost effectiveness of the treatment was estimated over 3 treatment periods: 1, 2 and 3.8 years. The cost-effectiveness ratios varied between SEK14,148 and SEK33,033 per life-year gained ($US1 = SEK7.70. Pounds 1 = SEK12.40) for the 3 treatment periods. Adding ramipril to conventional treatment for heart failure after acute myocardial infarction is therefore cost effective, and compares favourably with the cost effectiveness of other common medical therapies in the cardiovascular field.
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Seventeen patients were enrolled into the study. Mean age at study enrollment was 26.4+/-5.2 years. Mean baseline RVEF was 44+/-6.5%, mean RVEDV was 206.3+/-75.5 ml. Eight patients were randomized to the treatment group and 9 patients were randomized to the placebo group. RVEF did not improve in the Ramipril group from baseline to 1 year (43.8+/-7.1% vs. 40.9+/-13.3%, p=0.52) and remain unchanged in the placebo group (44.3+/-6.3 vs. 46.3+/-9.6%, p=0.42). RVEDV (184.5+/-56.4 ml vs. 179.6+/-66.4 ml, p=0.64) and RVESV (109.5+/-19.4 ml vs. 111.8+/-30.1, p=0.74) remained unchanged in the Ramipril group from baseline to 1 year as well as in the placebo group (228.1+/-89.2 ml vs. 204.5+/-50.4 ml, p=0.42 and 117.5+/-36.9 ml vs. 117.4+/-26.2 ml, p=0.99, respectively).
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The effect of various doses of the new angiotensin-converting enzyme inhibitor HOE 498 was compared with that of placebo in patients with mild essential hypertension. When a single dose of 2.5 mg of the drug was given, blood pressure was not significantly reduced despite a fall in converting enzyme levels. Single doses of 5 or 10 mg did reduce blood pressure, but complete inhibition of converting enzyme was apparent only with the 10-mg dose. Acute administration of a 20-mg dose proved to be unsuitable, since this was associated with too large a fall in pressure and the occurrence of symptomatic orthostatic hypotension. Although converting enzyme and blood pressure tended to recover in part 12 h after administration of the drug, both variables remained low even after 48 h.
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Captopril, enalapril, lisinopril, ramipril, cilazipril, and quinipril have all been documented to induce cough with an estimated frequency of at least 15% of treated patients. Common descriptors include tickling, dry, nonproductive, and persistent. Onset usually occurs during the first week of therapy and lasts as long as the drug is taken, remitting within a few days after the agent is discontinued. Alternative angiotensin-converting enzyme (ACE) inhibitors replicate the cough. The mechanism seems related to stimulation of lung afferent C fibers, perhaps by prostaglandin E2. It may also be related to decreased breakdown of substance P, the neurochemical mediator of the cough reflex released in response to stimulation of C fibers and metabolized by ACE. The possible role of prostaglandins is supported by two anecdotal reports of cough disappearing in patients receiving nonsteroidal antiinflammatory agents. Future trials should recognize cough as a side effect of ACE inhibitor therapy, and prospective determination of its true frequency and cross-occurrence are necessary.
There were 276 hip and pelvic fractures during a mean of 4.6 years of follow-up. Participants with baseline albuminuria had a significantly increased risk of fracture compared with participants without albuminuria (unadjusted hazard ratio=1.62 [1.22, 2.15], P<0.001; adjusted hazard ratio=1.36 [1.01, 1.84], P=0.05). A dose-dependent relationship was observed, with macroalbuminuria having a large fracture risk (unadjusted hazard ratio=2.01 [1.21, 3.35], P=0.007; adjusted hazard ratio=1.71 [1.007, 2.91], P=0.05) and microalbuminuria associating with borderline or no statistical significance (unadjusted hazard ratio=1.52 [1.10, 2.09], P=0.01; adjusted hazard ratio=1.28 [0.92, 1.78], P=0.15). Estimated GFR was not a predictor of fracture in any model, but rapid loss of estimated GFR over the first 2 years of follow-up predicted subsequent fracture (adjusted hazard ratio=1.47 [1.05, 2.04], P=0.02).
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Na+-H+ exchanger isoform-1 and NBC-1 gene expression were determined by reverse transcription polymerase chain reaction and Northern blot analysis; protein levels by Western blot analysis; and activity by measurement of H+ transport in left ventricular (LV) free wall, interventricular septum (IS) and right ventricle (RV) after induction of MI. Rats were treated with placebo, the angiotensin-converting enzyme inhibitor ramipril (1 mg/kg/day), the AT1 receptor antagonist valsartan (10 mg/kg/day) or the AT2 receptor antagonist PD 123319 (30 mg/kg/day). Treatment was started seven days before surgery.
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Case report A 28 year old gentleman presented after an episode of collapse with loss of consciousness. He gave a history of non-specific malaise and myalgia over the previous 7 days, with fever, a generalised rash and a non productive cough. He developed progressive shortness of breath with sharp, pleuritic chest pain that was unresponsive to antibiotics in the community.
It is not known whether physical exercise increases daily proteinuria in patients with proteinuric nephropathies, thus accelerating progression of the renal lesion. This study evaluates the acute effects of physical exercise on proteinuria in young adults with immunoglobulin A (IgA) nephropathy.
Inhibitors of the angiotensin-converting enzyme (ACE) decrease angiotensin II production and activate an intracellular signaling cascade that affects gene expression in endothelial cells. Because ACE inhibitors have been reported to delay the onset of type 2 diabetes, we determined ACE signaling-modulated gene expression in endothelial cells and adipocytes. Using differential gene expression analysis, several genes were identified that were 3-fold up- or down-regulated by ramiprilat in cells expressing wild-type ACE versus cells expressing a signaling-dead ACE mutant. One up-regulated gene was the cellular retinol-binding protein 1 (CRBP1). In adipocytes, the overexpression of CRBP1 enhanced (4- to 5-fold) the activity of promoters containing response elements for retinol-dependent nuclear receptors [retinoic acid receptor (RAR) and retinoid X receptor (RXR)] or peroxisome proliferator-activated receptors (PPAR). CRBP1 overexpression also enhanced the promoter activity (by 470 +/- 40%) and expression/release of the anti-inflammatory and antiatherogenic adipokine adiponectin (cellular adiponectin by 196 +/- 24%, soluble adiponectin by 228 +/- 74%). Significantly increased adiponectin secretion was also observed after ACE inhibitor treatment of human preadipocytes, an effect prevented by small interfering RNA against CRBP1. Furthermore, in ob/ob mice, ramipril markedly potentiated both the basal (approximately 2-fold) and rosiglitazonestimulated circulating levels of adiponectin. In patients with coronary artery disease or type 2 diabetes, ACE inhibition also significantly increased plasma adiponectin levels (1.6- or 2.1-fold, respectively). In summary, ACE inhibitors affect adipocyte homeostasis via CRBP1 through the activation of RAR/RXR-PPAR signaling and up-regulation of adiponectin. The latter may contribute to the beneficial effects of ACE inhibitors on the development of type 2 diabetes in patients with an activated renin-angiotensin system.
Data from German Health Examination Surveys (GNHIES98 1998, n = 7,124 and DEGS1 2008-2011 n = 7,988, age 18-79 years) including standardized blood pressure (BP) measurements and Anatomical Therapeutic Chemical (ATC) medication codes were analyzed.
The study was stopped 6 months early (after 4.5 years) by the independent data safety and monitoring board because of a consistent benefit of ramipril compared with placebo. Ramipril lowered the risk of the combined primary outcome by 25% (95% CI 12-36, p=0.0004), myocardial infarction by 22% (6-36), stroke by 33% (10-50), cardiovascular death by 37% (21-51), total mortality by 24% (8-37), revascularisation by 17% (2-30), and overt nephropathy by 24% (3-40, p=0.027). After adjustment for the changes in systolic (2.4 mm Hg) and diastolic (1.0 mm Hg) blood pressures, ramipril still lowered the risk of the combined primary outcome by 25% (12-36, p=0.0004).
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DNA damage in the peripheral blood leukocytes (PBL) of patients with coronary artery disease (CAD) was investigated using the sensitive alkaline single cell gel electrophoresis (SCGE)/comet assay.This case-control study consisted of CAD patients (n = 200; mean age, 59.04 ± 0.75 years) undergoing treatment at local hospitals and age-, sex-, and ethnicity-matched healthy controls (n = 200; mean age, 57.88 ± 0.96 years) from the general population.CAD patients had significantly (P < 0.001) increased DNA damage (tail DNA percent (T-DNA %) 22.45 ± 0.50 versus 5.81 ± 0.28; tail moment (TM) 89.35 ± 3.16 versus 9.98 ± 0.69; Olive tail moment (OTM) 60.50 ± 1.79 versus 10.94 ± 0.63; damage frequency (DF) 91.12 ± 0.93 versus 41.78 ± 2.04, damage index (DI) 173.68 ± 3.36 versus 48.53 ± 2.59) compared to controls. Patients with acute myocardial infarction (AMI) showed significantly higher DNA damage than patients with unstable angina (UA) (T-DNA % 24.05 ± 0.87 versus 21.06 ± 0.90; TM 100.02 ± 6.19 versus 81.61 ± 5.84; OTM 66.19 ± 3.20 versus 56.47 ± 3.33; DF 94.02 ± 0.84 versus 91.10 ± 1.16, DI 184.13 ± 5.33 versus 166.42 ± 5.89). Moreover, DNA damage was found to be significantly (P < 0.05) elevated in patients receiving ecosprin, ramipril, and metoprolol therapy compared to aspirin and nitrocontin.The increased DNA damage in CAD patients may be the consequence of disease and/or drug therapy. These observations are of concern because unrepaired DNA can lead to malignancy, and the likelihood of increasing mortality and morbidity rates in CAD patients.