Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0432222 (SEM)
 47,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of celiprolol on insulin sensitivity, glucose tolerance and serum lipids were compared to those of other antihypertensive drugs (beta- or Ca-blocker or ACE-inhibitor) in 23 dyslipidemic non-diabetic patients with controlled hypertension. Hyperinsulinemic euglycemic clamp and independent oral glucose tolerance tests (OGTT) were performed before and 6 months after the study treatment. Six patients out of 23 were randomized to the control group where antihypertensive monotherapy was kept unchanged. Mean glucose disposal rate (M, mean +/- SEM) determined in the clamp test increased in the celiprolol group from 24.4 +/- 2.3 to 34.9 +/- 2.4 mumol/kg/min (p < 0.001). Insulin sensitivity improved during celiprolol treatment independent of the previous treatment. In the control group, M remained practically unchanged (21.6 +/- 3.7 mumol/kg/min). During 2 h OGTT, incremental glucose and insulin AUC decreased in the celiprolol group from 4.5 +/- 0.7 to 2.0 +/- 0.6 mM*h (p < 0.002) and from 113 +/- 16 to 72 +/- 10 mU/l*h (p < 0.005), respectively. There was also a small beneficial change in serum lipids in the celiprolol group: a reduction in serum total cholesterol (-4%), triglycerides (-11%) and LDL-cholesterol (-9%), and an increase in HDL-cholesterol (+6%) and HDL/LDL ratio (+15%). No significant change occurred in the control group. Fasting serum glucose and insulin did not change significantly in either group. In this study with a limited control group, celiprolol improved insulin sensitivity, glucose tolerance and serum lipid profiles of dyslipidemic hypertensive patients.
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PMID:Effects of celiprolol on insulin sensitivity and glucose tolerance in dyslipidemic hypertension. 759 14

The aim of this study was to evaluate whether markers of collagen synthesis, hyaluronan (HA) and procollagen type III aminoterminal peptide (PIIINP) in bronchoalveolar lavage fluid (BALF) and serum (S) were correlated to paraclinical markers of disease activity (S-ACE, S-IgG S-IgA S-calcium, chest X-ray (CXR) profusion score, pulmonary function tests (FEV1, FVC, TLC, DLCO)) in pulmonary sarcoidosis. The material comprised 48 patients with biopsy proven sarcoidosis (35 male, 13 female, median age 31 years) and 24 controls (16 male, 8 female, median age 60 years). BAL was performed in the right middle lobe with 250 ml saline. Patients had higher BALF-HA, mean 88 +/- 13 (SEM) micrograms/l, than controls, 39 +/- 2 micrograms/l (p < 0.01), higher BALF-albumin, 121 +/- 13 mg/l, than controls 58 +/- 4 mg/l (p < 0.01), and higher BALF/S-HA ratio, 3.35 +/- 0.51, than controls, 1.23 +/- 0.60 (p < 0.01). There were no significant differences for S-HA, BALF-PIIINP, or S-PIIINP. In patients significant correlations were found between BALF-HA, S-HA, and BALF-albumin; between S-HA and S-ACE; between BALF/S-HA and BALF-albumin; between CXR profusion score and S-HA, S-ACE, S-IgG, S-IgA, FEV1, FVC, TLC and DLCO. The results indicate that measurement of S-HA, BALF-HA, and BALF-albumin may be of value in the monitoring of disease in pulmonary sarcoidosis.
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PMID:Hyaluronan and procollagen type III aminoterminal peptide in serum and bronchoalveolar lavage fluid in patients with pulmonary sarcoidosis. 761 74

The presence of constituents of the renin-angiotensin system (RAS) in ocular tissues and fluids suggests this system is involved in ocular physiology. Angiotensin II (AngII) is the main biological effector of the system, so we measured AngII in plasma and in aqueous humor of the anterior ocular chamber of patients undergoing cataract extraction. Untreated normotensive patients were compared with arterial hypertensive patients taking either diuretics which stimulate the RAS or angiotensin converting enzyme (ACE) inhibitors which reduce the production of AngII. Plasma levels of AngII were higher in patients on diuretics (5.46 +/- 1.04 fmol/ml; mean +/- SEM) than in untreated cataract patients (2.28 +/- 0.32 fmol/ml, p < 0.02), and were very low with ACE inhibitors (0.51 +/- 0.18 fmol/ml). In aqueous humor, AngII was measurable in 7 of 11 patients on diuretics (median 1.1 fmol/ml), and in 6 of 16 normotensive patients (median < 0.55 fmol/ml), but not in aqueous humor of 4 patients receiving enalapril or captopril. These results demonstrate the presence of AngII in the eye but do not exclude either its sequestration in the eye or local production. The possibility of individual measurements of intraocular AngII will permit more precise determination of its role in future studies.
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PMID:Individual measurements of angiotensin II concentrations in aqueous humor of the eye. 771 76

The effects of two types of angiotensin converting enzyme (ACE) inhibitors, enalapril (long-acting) and captopril (short-acting), on serum electrolytes and circadian rhythm of urinary electrolyte excretions were compared in relation to aldosterone status in patients with essential hypertension and normal renal function. Enalapril (5 mg once daily) and captopril (12.5 mg t.i.d.) were administered to 11 patients for 1 week each in a crossover fashion. Blood sampling in the early morning and 4-hour split urinary sampling for 24 hours were performed on the last day of control and each treatment periods. Enalapril and captopril significantly reduced blood pressure to similar levels. Enalapril but not captopril significantly inhibited plasma aldosterone concentration and urinary aldosterone excretion. Neither drug apparently altered serum or urinary Na levels. Both drugs significantly decreased urinary K excretion (p < 0.05, control: 44 +/- 4 mEq/day, captopril: 39 +/- 2 mEq/day, enalapril: 39 +/- 2 mEq/day; mean +/- SEM), but did not significantly alter serum K level (control: 4.1 +/- 0.1 mEq/l, captopril 4.2 +/- 0.2 mEq/l, enalapril 4.3 +/- 0.1 mEq/l). The circadian rhythm (acrophase) of urinary K excretion was not affected by either drug, while the amplitude was decreased by both, as assessed by the cosinor method. In summary, although enalapril caused more sustained inhibition of aldosterone secretion compared with captopril, both drugs showed similar effects on the K homeostasis in patients with mild essential hypertension.
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PMID:Crossover comparison of the effects of enalapril and captopril on potassium homeostasis in patients with mild hypertension. 788 4

The effect of chronic angiotensin converting enzyme (ACE) inhibition on the incidence of fatal ventricular fibrillation during regional myocardial ischaemia and reperfusion is not known. A reduction in cardiac angiotensin II and/or a vagomimetic response may result in antiarrhythmic activity. Pigs pre-treated with the ACE inhibitor trandolapril 0.3 mg.kg-1 or placebo orally for 10 days were subjected to thoracotomy. The left anterior descending coronary artery was ligated (CAL) for 20 min and reperfused for 45 min. Trandolapril decreased cardiac ACE activity and prevented the fall in the ventricular fibrillation threshold (VFT) during ischaemia: after 5 min of ischaemia the VFT in the trandolapril group was 25.5 +/- 4.6 mA (mean +/- SEM) vs 13.1 +/- 2.2 mA in the placebo group (P < 0.05). Trandolapril also decreased the incidence of spontaneous ventricular fibrillation during reperfusion to 1/6 vs 6/7 in the placebo group (P < 0.05). Heart rate in the trandolapril group fell. During ischaemia, trandolapril increased blood flow in the non-ischaemic zone, but decreased blood flow in the central ischaemic zone of the left ventricle. Similarly it decreased tissue levels of phosphocreatine in this zone. During reperfusion trandolapril increased blood flow both in non-ischaemic and central ischaemic zones. Chronic oral pre-treatment with trandolapril resulted in marked antifibrillatory effects which were associated with inhibition of cardiac ACE activity and a decreased heart rate.
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PMID:Chronic oral pretreatment with the angiotensin converting enzyme inhibitor, trandolapril decreases ventricular fibrillation in acute ischaemia and reperfusion. 792 22

The progression of diabetic nephropathy can be positively influenced by maintaining a low blood pressure level. This has been shown in studies with conventional antihypertensive treatment as well as with ACE inhibitors. Whether the latter group of drugs is more effective remains to be proven and was the aim of our study. In a prospective randomized study we compared the effects of ACE inhibition and beta-blockade on retarding progression of renal function in IDDM patients with an early stage of overt diabetic nephropathy. Twenty-nine patients were studied for 2 years, 15 were randomized for treatment with captopril and 14 for atenolol. Every 6 weeks blood pressure and urinary albumin and total protein excretion were measured. GFR was measured every 6 months as 51Cr-EDTA clearance. Baseline values for blood pressure, renal function and albuminuria were identical in the two groups. The effect of both drugs on blood pressure was not significantly different. In the captopril-treated patients MAP before and after 2 years was 110 +/- 3 (SEM) and 100 +/- 2 mm Hg, respectively and in the atenolol-treated patients 105 +/- 2 vs 101 +/- 2 mm Hg. Both drugs reduced albuminuria and total proteinuria to the same extent. With captopril albuminuria decreased from 1549 (989-2399) to 851 (537-1380) mg/24 h and proteinuria from 2.5 (1.6-3.8) to 1.2 (0.8-1.8) g/24 h. With atenolol albuminuria decreased from 933 (603-1445) to 676 (437-1047) mg/24 h and proteinuria from 1.5 (1.0-2.4) to 0.9 (0.6-1.5) g/24 h.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Captopril and atenolol are equally effective in retarding progression of diabetic nephropathy. Results of a 2-year prospective, randomized study. 774 19

Anaphylactoid reactions (AR) are the most feared complications of hemodialysis. Recently, a high incidence of AR has been reported during dialysis with AN69 membranes in patients treated with ACE inhibitors. Plasma levels of C3a, histamine and bradykinin were measured in 12 patients at the onset of AR during dialysis with AN69. We also investigated bradykinin generation in 10 symptom-free patients dialyzed with four different membranes. None of the 12 patients studied during AR displayed excessive complement activation or histamine release. In contrast, high bradykinin plasma levels (2392 +/- 53 fmol/ml; mean +/- SEM) were observed in all nine patients of whom bradykinin was measured. One patient developed two consecutive episodes of hypersensitivity on AN69 membranes even without taking ACE inhibitors. Bradykinin levels were high in both episodes (5280 and 10467.7 fmol/ml). Furthermore, this patient showed no symptoms and normal bradykinin levels (123.4 fmol/ml) when dialyzed with other membranes. The role of the membrane type in the AR is further substantiated by the observation that AN69 also provoked a significantly higher bradykinin generation (327.6 +/- 18 fmol/ml; mean +/- SEM) during symptom-free sessions compared to other membranes like CuprophanR (5.1 +/- 7.3), HemophanR (17.2 +/- 6.3) and PolysulfoneR (39.7 +/- 6.6). Our findings strongly suggest that bradykinin is the principal mediator of AR during hemodialysis with AN69 membranes. To our knowledge it is the first time that data support the hypothesis of a more general role of bradykinin in shock-like symptoms. Furthermore, bradykinin generation must be regarded as a new marker of biocompatibility of extracorporeal treatments.
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PMID:Bradykinin is a mediator of anaphylactoid reactions during hemodialysis with AN69 membranes. 807 63

Persistent dry cough is one of the most common side-effects during therapy with ACE inhibitors. The frequency of cough ranges widely (from 0.2% to 15%) in different series, being higher in small studies and smaller in retrospective studies with large number of patients. The aim of the present study was to evaluate the true frequency of cough induced by treatment with ACE inhibitors in Greek hypertensives and to determine various possibly correlated parameters, including sex, duration of therapy and kind and dose of ACE inhibitors. All hypertensive patients followed in our Hypertension Clinic and treated with ACE inhibitors participated in the study. A total of 228 patients, 103 males and 125 females, 24-80 years of age, were treated with ACE inhibitors for a period of 1-41 months: 121 with enalapril, 40 with captopril, 39 with lisinopril, 25 with perindopril and 3 with ramipril. During treatment with ACE inhibitors persistent dry cough occurred in 15 patients, 12 women and 3 men, giving a frequency of 6.58%. Eleven patients (4.82%) volunteered the information and three after questioning. The mean age of these 15 patients with cough was significantly higher from that of the group (n = 213) without cough (64.27 +/- 2.5 vs. 57.9 +/- 0.74 years, mean +/- SEM, P = 0.024). The 12 women with cough were significantly older than the 113 without cough (67.77 +/- 2.8 vs. 57.8 +/- 1.04 years, P = 0.032).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Frequency of cough during therapy with ACE inhibitors in Greek hypertensives. 811 58

The purpose of this study was to determine whether angiotensin I-converting enzyme (ACE) is present in cultured bovine bronchial epithelial cells (BBECs) and whether its activity can be modulated. We found that extracts of confluent monolayers of cultured BBECs degraded [glycine-1-14C]hippuryl-L-histidyl-L-leucine at a rate of 843 +/- 66 pmol/hr/mg protein (mean +/- SEM, n = 5). In addition, we found that the enzyme was shed into the culture medium. ACE activity in BBECs was inhibited by three selective, but structurally different, ACE inhibitors (captopril, quinapril, and cisalaprilat) with an IC50 of approximately 2 nM. Increasing chloride concentration in the assay buffer resulted in an increase in BBECs ACE activity of 63%. Enzyme activity was also modulated by the presence of zinc cation in the assay buffer. Addition of dexamethasone to the culture medium was associated with a significant increase in BBECs ACE activity (P < 0.05), which was inhibited by the steroid receptor antagonist RU 38486. Western blot analysis of BBECs, tracheal and bronchial mucosal strips utilizing a cross-reacting rabbit anti-mouse ACE antibody, showed a faint 175 kDa band and additional strong 52 kDa and 47 kDa band. The mechanism of generation of the low M.W. bands is unknown. Our data indicate the presence of ACE in cultured BBECs and that enzyme activity can be modulated.
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PMID:Regulation of angiotensin I-converting enzyme in cultured bovine bronchial epithelial cells. 830 Jul 52

To determine the effect of ACE inhibitor therapy on lymphocyte beta-adrenoceptor function and density, as well as the in vivo myocardial response to beta-agonist stimulation, we studied 12 patients with chronic severe heart failure before and after 16 weeks' treatment with quinapril. Lymphocyte beta-adrenoceptor function (intracellular cAMP production in response to isoprenaline) was studied as a surrogate tissue for myocardium, and increased significantly after quinapril at concentrations of isoprenaline between 10(-3) and 50 mmol.l-1. Lymphocyte beta-adrenoceptor density (six patients) measured by [125I] iodocyanopindolol binding, increased from 242 +/- 72 (mean +/- SEM) to 884 +/- 17 receptors/cell (P < 0.05). Changes in functional myocardial beta-adrenoceptor status were determined by measuring changes in haemodynamic responses to exercise and to incremental dobutamine infusion. Following quinapril there were significant improvements in cardiac index, stroke volume and cardiac power output during sub-maximal exercise testing and dobutamine infusion; stroke work index in response to dobutamine (but not exercise) improved significantly. ACE inhibitors cause lymphocyte beta-adrenoceptor upregulation in heart failure, which is associated with an improved cardiac pumping capacity in response to beta-agonist stimulation.
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PMID:Lymphocyte beta adrenoceptor upregulation and improved cardiac response to adrenergic stimulation following converting enzyme inhibition in congestive heart failure. 838 98


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