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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The sustained increase in peripheral vascular resistance is the hemodynamic alteration characteristic of the established adult hypertension. This is the result of a vascular tone increase and/or structural changes which imply hypertrophy as well as hyperplasia of the vascular smooth muscle fibers, hypertrophy of the cardiac cells and an increase in the constituent synthesis of the extracellular matrix. Angiotensin II and noradrenalin exert major trophic effects which accelerate the progression of cardiovascular hypertrophy being the cardiovascular system very sensitive to the trophic actions of renin-angiotensin. Angiotensin II induces the expression of the A-chain of the growth factor of platelet origin, of the baseline fibroblastic growth factor and of the B-transformer factor and, moreover, stimulates type I and type III collagen synthesis and favors trophic factors release. Therefore, the renin-angiotensin system plays an important role in growth regulation and myocyte remodelation and in the cardiovascular extracellular matrix which is mediated through specific receptors, since it can be inhibited by ATI receptor antagonists for angiotensin II and ACE. Cilazapril is an ACE long duration agent which produces a reduction of both blood pressure and cardiovascular hypertrophy. This is a multiple action mechanism exerting a vasodilator action, inhibiting the sympathetic tone or increasing kinine levels and inhibiting the cardiac and vascular renin-angiotensin system.
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PMID:[Effect of cilazapril, a converting enzyme inhibitor, on cardiovascular hypertrophy in the hypertensive patient]. 873 37

The effects of long-term monotherapy with cilazapril, an angiotensin-converting enzyme inhibitor, on blood pressure, glucose tolerance, and serum lipid profiles were prospectively investigated in 66 patients with hypertension: 23 with normal glucose tolerance and 43 with glucose intolerance (including 9 patients with non-insulin-dependent diabetes mellitus). The levels of plasma glucose, serum insulin, serum lipids, glycated hemoglobin A(lc) (Hb A(lc)), and fructosamine were determined before and during long-term (mean +/- SD, 26.2 +/- 1.2 weeks) therapy with cilazapril. A 75-g oral glucose tolerance test was performed before and during treatment. Significant reductions in both systolic and diastolic blood pressures in both patient groups were maintained during the study. Neither fasting nor post-glucose load venous plasma glucose levels were altered in either group of patients, and no patient with normal glucose tolerance developed diabetes mellitus during the study. There was no significant change in the insulinogenic index (delta serum insulin/delta venous plasma glucose at 30 minutes post-glucose load) in either group, and glucose intolerance was slightly improved with significant reductions (P < 0.01) in Hb A(lc) and fructosamine in the patient group with impaired glucose tolerance. Serum total cholesterol (TC), low-density lipoprotein cholesterol, and triglyceride levels were significantly (P < 0.01) decreased and high-density lipoprotein cholesterol levels increased in patients with hypercholesterolemia (TC levels > or = 5.69 mmol/L). These results suggest that long-term cilazapril therapy may improve glucose and lipid metabolism in hypertensive patients with impaired glucose tolerance. Cilazapril also appears to be useful as an antihypertensive agent for hypertensive patients with either impaired glucose tolerance or hypercholesterolemia.
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PMID:Effect of cilazapril therapy on glucose and lipid metabolism in patients with hypertension. 875 Apr 4

Numerous antihypertensive drugs exist with different modes of action, which have a really effective impact on hypertension. The life expectancy of hypertensive patients is known to depend on the degree of damage caused to their target organs by the hypertension itself. Cardiovascular hypertrophy and its complications are considered to be among the major elements of this process. This work evaluates the effectiveness of the long-term treatment of essential hypertensive subjects (n = 10) with a long-acting ACE-inhibitor, cilazapril, as concerns their blood pressure and cardiac hypertrophy. Cilazapril given orally in a daily dose of 2.5 mg effectively lowered both the systolic (delta 30 mm Hg) and the diastolic (delta 19 mm Hg) blood pressure. No changes were found in body weight or heart rate, and only one side-effects (skin rash) was reported. Cilazapril considerably decreased the left ventricular mass and hence the hypertrophic index of hypertensive patients with cardiac hypertrophy, suggesting that ACE inhibitors are effective not only in lowering blood pressure and decreasing hypertrophy, but also in lowering the cardiac morbidity and mortality.
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PMID:[Effect of cilazapril in patients with essential hypertension: effect on cardiac hypertrophy]. 875 70

We examined effects of salt and cilazapril on the Ca pump and Na/Ca exchange system in arterial smooth muscle of Dahl salt-sensitive (DS) rats. Twenty-four DS rats were assigned to four groups. H and H+ rats were fed a high salt diet; L- and L+ rats were fed a low salt diet. H+ and L+ were administered cilazapril. Aortic rings were superfused with physiologic saline and isometric tension was measured. Relaxation of low Na+-induced contraction was promoted by the removal of external Ca. Cilazapril significantly decreased blood pressure in both the high and low salt diet groups. The inhibition of renin-angiotensin system by cilazapril showed that Ca extrusion by ATP-driven Ca pump was decreased by salt loading, and that Ca extrusion by Na/Ca exchange was increased by salt loading. There was a negative correlation between Ca extrusion by Ca pump and blood pressure, and a positive correlation between Ca extrusion by Na/Ca exchange and blood pressure. These results suggest that the decrease of Ca2+ extrusion by ATP-driven Ca pump resulting from a high salt diet might lead to an elevation in the concentration of cellular Ca2+ and contribute to the mechanism of hypertension in DS rats, and that Ca2+ extrusion by the Na/Ca exchange might be increased in compensation for an increase in cellular Ca2+ concentration on the high salt diet.
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PMID:Effect of cilazapril and salt on Ca2+ extrusion in arterial smooth muscle of Dahl rats. 916 Jul 92

We investigated the efficacy of an Angiotensin Converting Enzyme [ACE] inhibitor on daytime and night-time blood pressure in 55 male hypertensive patients with moderately severe to severe obstructive sleep apnea. We resolved to determine if treatment oriented towards the reduction of hypertension would be successful, despite persistent repetitive hypoxemia and sleep-disordered breathing. The study was a randomized, double-blind, single daily dose, placebo-controlled protocol, with 8 days drug intake (placebo or 2.5 mg Cilazapril) and monitoring on the final day of drug administration. Subjects underwent continuous 24-h arterial blood pressure monitoring during baseline and treatment conditions. Polysomnography was performed at night during the 24-h arterial monitoring period. Cilazapril (2.5 mg) lowered systolic, diastolic and mean blood pressure, despite persistence of repetitive obstructive apneas during sleep and the associated repetitive hypoxemia. The lowering of blood pressure occurred without a significant change in heart rate, and was noted during nocturnal sleep, performance testing and graded exercise.
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PMID:Effect of angiotensin converting enzyme inhibition [Cilazapril] on blood pressure recording in hypertensive obstructive sleep apneic patients. 929 11

Using Otsuka Long-Evans Tokushima Fatty (OLETF) rats, a new model of human non-insulin-dependent diabetes mellitus (NIDDM), we examined the role of local angiotensin II in cardiovascular and renal complications of NIDDM. OLETF rats were orally given cilazapril (an angiotensin-converting enzyme inhibitor, 1 or 10 mg/kg), E4177 (an angiotensin AT1 receptor antagonist, 10 mg/kg), or vehicle for 26 or 40 weeks (from the age of 20 to 46 or 60 weeks). Cardiac mRNAs were measured by Northern blot analysis, and the thickening of the coronary arterial wall and the degree of perivascular fibrosis were determined by an image analyzer. Cilazapril or E4177 did not significantly affect body weight or plasma glucose and insulin levels of OLETF rats, indicating the minor effects on diabetes itself. However, both drugs significantly and similarly prevented coronary microvascular remodeling (the increase in wall thickening and perivascular fibrosis in coronary arterioles and small coronary arteries) in OLETF rats, and they were associated with the suppression of cardiac transforming growth factor-beta1 expression. Both drugs suppressed not only the increase in left ventricular weight but also the downregulation of cardiac alpha-myosin heavy chain expression in OLETF rats. Glomerulosclerosis and glomerular hypertrophy in OLETF rats were improved by cilazapril and E4177 to a comparable extent. These results, taken together with the fact that OLETF rats show normal plasma renin levels, support that the AT1 receptor is involved in the pathogenesis of cardiac and renal complications in NIDDM.
Hypertension 1997 Nov
PMID:Angiotensin blockade improves cardiac and renal complications of type II diabetic rats. 936 55

alpha-Adrenergic blockers are potential alternative antihypertensive agents for diabetic patients. Data on their relative efficacy and their effect on kidney function and albuminuria are very limited however. 76 patients with diabetes type 2, hypertension (>/=140/90 mm Hg) and albuminuria (>/=30 mg/24 h) were randomized into three groups to receive cilazapril (2.5-10 mg), doxazosin (2-8 mg) or both. Patients of the first and second groups received a single agent for 4 months, the agents were then crossed for an additional period of 4 months followed by the addition of hydrochlorothiazide (25 mg) for a third 4-month period. Blood pressure was monitored monthly, creatinine clearance and HbA1c were measured before and at the end of each treatment period. Patients of the third group received reduced doses of cilazapril and doxazosin for 4 months. Hydrochlorothiazide was then added for the subsequent 4 months. There was a significant decline in blood pressure values during the first period in all groups. Cilazapril: systolic blood pressure (SBP) 160 +/- 6 to 149 +/- 5 mm Hg; diastolic blood pressure (DBP): 101 +/- 3 to 94 +/- 3 mm Hg (p = 0.001). Albuminuria declined from 350 +/- 105 to 205 +/- 96 mg/24 h (p = 0.001), creatinine clearance (CrCl) was unchanged. Doxazosin: SBP: 160 +/- 7 to 151 +/- 6 mm Hg; DBP: 97 +/- 4 to 90 +/- 4 mm Hg (p = 0.001). Albuminuria 373 +/- 121 to 322 +/- 107 mg/24 h (p = 0.065) and CrCl 87 +/- 7 to 91 +/- 6 ml/min. The combination of both agents at half doses was equipotent or superior to either drug alone. Cross-over of cilazapril and doxazosin reproduced the hypotensive effect and reversed the antialbuminuric effect. The addition of hydrochlorothiazide resulted in a further decline of 6-14 mm Hg in SBP and 3-11 mm Hg in DPB.
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PMID:Effect of an alpha-adrenergic blocker, and ACE inhibitor and hydrochlorothiazide on blood pressure and on renal function in type 2 diabetic patients with hypertension and albuminuria. A randomized cross-over study. 973 16

Disorders in peripheral microcirculation are observed in arterial hypertension and may be improved by antihypertensive treatment. In this pilot study the authors measured capillary blood cell velocity in the finger nailfold in 14 patients (mean age 50 +/- 14 years, range 30-71 years; 9 men, 5 women) with mild-to-moderate essential hypertension. After a 3-week placebo period, patients received double-blind randomized treatment with either 0.2- to 0.4-mg moxonidine (n=7) or 2.5- to 5.0-mg cilazapril (n=7). Finger nailfold video capillaroscopy was performed at baseline and after 8 weeks of treatment. Blood pressure was measured by conventional office technique. Capillary blood cell velocity, 1 minute after local finger cooling, increased in the Moxonidine group (0.65 +/- 0.53 mm/sec to 1.13 +/- 0.77 mm/sec; p<0.05) after 8 weeks treatment compared to the baseline. The increase in the Cilazapril group from 0.79 +/- 0.45 mm/sec to 0.93 +/- 1.03 mm/sec did not reach a level of statistical significance. Blood pressure decreased from 151 +/- 8/101 +/- 5 to 147 +/- 6/98 +/- 7 mmHg in the Moxonidine group and from 164 +/- 12/102 +/- 6 to 140 +/- 9/93 +/- 9 mmHg in the cilazapril group. Moxonidine increased nailfold capillary blood cell velocity 1 minute after local finger cooling in patients with mild-to-moderate hypertension. This improvement of the peripheral microcirculation may be associated with reversal of vascular dysfunction in hypertension.
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PMID:Effect of moxonidine and cilazapril on microcirculation as assessed by finger nailfold capillaroscopy in mild-to-moderate hypertension. 982 45

The intrarenal factors responsible for hypertension in double-transgenic rats (dTGR) harboring human renin and human angiotensinogen genes are unclear. The pressure-natriuresis and -diuresis relationships in response to chronic angiotensin-converting enzyme (ACE) inhibition and AT1 receptor blockade were evaluated. Renal renin-angiotensin and nitric oxide (NO) system gene expression was also investigated. Six-week-old dTGR were treated for 3 wk with submaximal doses of cilazapril (10 mg/kg, orally) or losartan (10 mg/kg, orally) or with the drug combination. In untreated dTGR, pressure-natriuresis relationships were maximally shifted rightward by approximately 70 to 80 mmHg, and both renal blood flow (RBF) and GFR were markedly decreased. Submaximal cilazapril and losartan dosages both decreased systolic BP by 30 mmHg and shifted the pressure-natriuresis curves leftward by 25 to 30 mmHg. Cilazapril increased RBF and GFR to values observed in normotensive control animals but did not significantly affect fractional sodium excretion (FENa) or fractional water excretion (FEH2O) curves. In contrast, losartan had no significant effect on RBF or GFR but shifted the FENa and FEH2O curves leftward. The cilazapril and losartan combination completely normalized BP and shifted the pressure-natriuresis curves leftward more than did either drug alone. When cilazapril and losartan were administered at higher doses (30 mg/kg, orally), the two drugs equally shifted the pressure-natriuresis curves leftward, by 50 mmHg. Both drugs increased RBF and GFR; however, only losartan shifted FENa and FEH2O curves leftward. Human and rat renin and angiotensinogen genes were downregulated in dTGR and were increased by losartan and cilazapril treatments, whereas no changes in the expression of rat ACE and AT1A receptor genes were observed. Endothelial NO synthase expression was increased by cilazapril but not by losartan. Neither inducible NO synthase nor neural NO synthase gene expression was affected by drug treatments. Therefore, submaximal ACE inhibition enhanced sodium excretion mainly by increasing RBF and GFR, whereas submaximal AT1 receptor blockade decreased tubular sodium and water reabsorption. The combination of the two drugs produced an additive effect. The ACE inhibitor effects may involve increased endothelial NO synthase expression, perhaps related to the inhibition of bradykinin degradation.
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PMID:Angiotensin-converting enzyme inhibition and AT1 receptor blockade modify the pressure-natriuresis relationship by additive mechanisms in rats with human renin and angiotensinogen genes. 1044 34

Male patients with arterial hypertension and obstructive sleep-related breathing disorders (mean age 50 y, Body Mass Index (BMI) 32.4 kg m-2, Respiratory Disturbance Index (RDI) 47.2 and systolic/diastolic blood pressure (SBD/DBD) 162/103 mmHg) were examined before and after 8 days of treatment with the long-acting angiotensin-converting-enzyme (ACE) inhibitor cilazapril 2.5 mg vs. placebo in a double-blind design with parallel groups. Cardiorespiratory polysomnography was carried out at night; during daytime wakefulness patients submitted to examinations of physical and mental exertion. Cilazapril reduced the mean pressure during the entire examination period (day and night) by 9.55 (SD +/- 7.13) mmHg, compared to 4.57 (SD +/- 7.20) mmHg for placebo (P < 0.006), independently from systematic changes of heart rate (x = -3.3 and -3.5 bpm, respectively). During REM sleep, mean arterial pressure was significantly reduced by 8.63 (SD +/- 10.1) mmHg, compared to a reduction on placebo of 3.17 (SD 9.6) mmHg (P = 0.023). Under psychometric strain, the mean arterial pressure was reduced by 15.31 (SD +/- 8.7) mmHg with cilazapril; under placebo medication by 6.19 (SD +/- 7.3) mmHg (P < 0.0001). Heart rate was not significantly changed.
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PMID:Arterial hypertension and sleep apnoea: effect of the angiotensin-converting enzyme (ACE) inhibitor cilazapril on continuously measured blood pressure during sleep and wakefulness. 1060 86


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