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

Thirty-five patients with mild hypertension (WHO Class I) participated in a double-blind cross-over study involving two 8-week periods of treatment with cilazapril 2.5-5 mg once daily or hydrochlorothiazide 25-50 mg once daily, in each case preceded by a 4-week placebo period. Thirty-two patients completed the study, the aim of which was to compare the effects of the drugs on serum electrolyte levels, left ventricular mass and cardiac arrhythmias, as assessed by echocardiography and 48-h Holter monitoring. Both drugs significantly reduced systolic (P < 0.01) and diastolic (P < 0.001) blood pressures (comparisons with placebo periods). Cilazapril and hydrochlorothiazide had opposite effects on ventricular ectopic activity. The beneficial effect of cilazapril on ventricular extrasystole counts correlated significantly (P < 0.001) with the reduction of left ventricular mass index. Hydrochlorothiazide had no effects on left ventricular mass or diastolic function. Serum potassium values were significantly (P < 0.001) reduced by hydrochlorothiazide but there was no correlation between changes in potassium levels and changes in ventricular ectopic activity. The results of the study suggest that hydrochlorothiazide and cilazapril were equally effective in reducing blood pressure, but only cilazapril reduced left ventricular hypertrophy and suppressed ventricular ectopic activity.
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PMID:Left ventricular mass, serum electrolyte levels and cardiac arrhythmias in patients with mild hypertension treated with cilazapril or hydrochlorothiazide. 750 25

In 13 normotensive subjects on a normal sodium diet, we studied hormonal, blood pressure, and renal vascular changes and dextran sieving profiles induced by infusion of exogenous angiotensin II (Ang II) (5 ng.kg-1.min-1). during baseline conditions and after 5 days of administration of the angiotensin converting enzyme inhibitor cilazapril. Cilazapril induced a renal vasodilative effect without affecting supine blood pressure and glomerular filtration rate. Fractional dextran clearances were significantly decreased for dextran of effective radius ranging from 3.0 to 4.0 nm. This shift was primarily related to an increase in glomerular capillary plasma flow, because no change was observed in the transcapillary glomerular pressure gradient, the ultrafiltration coefficient, or the membrane parameters. Ang II elicited a slight pressor response accompanied by hormonal, antinatriuretic, and renal hemodynamic changes that were similar during and before short-term angiotensin converting enzyme inhibition. Dextran sieving curves were unchanged by a low dose of Ang II. However, the transcapillary glomerular pressure gradient and the ultrafiltration coefficient were computed to increase by 19.4% and to decrease by 44.2%, respectively, whereas membrane parameters were unaffected. When superimposed onto short-term angiotensin converting enzyme inhibition, glomerular response to this unique dose of Ang II was similar to that induced by Ang II alone. These findings indirectly suggest that most, if not all, of the renal effects of cilazapril are mediated through suppression of Ang II formation.
Hypertension 1993 Mar
PMID:Renal response to angiotensin after short-term angiotensin converting enzyme inhibition. 768 91

To assess the effectiveness of cilazapril in regulating blood pressure (BP) in patients with sleep-related breathing disorders, 23 male patients (mean age, 50 years; mean body mass index, 32.7 kg/m2) with a mean apnea/hypopnea index of 49.7 and arterial hypertension (163/104 mm Hg) participated in a placebo-controlled, randomized, double-blind study. They received either cilazapril, 2.5 mg/day (n = 12) or placebo (n = 11). The effects of treatment were studied under different conditions of sleep and physical and mental load before and after 8 days of treatment. Measurements by night included cardiorespiratory polysomnography, inductive plethysmography, pulse oximetry and nasal air flow, electroencephalography, (EEG), electrooculography and electromyography, (ECG), and blood pressure (BP). Measurements by day (ECG, heart rate, and BP) were performed at rest and under physical and mental load. Systolic, diastolic, and mean BP (5 min at night; 1 s during the day), heart rate, apnea and hypopnea index, EEG data, and test reaction times were compared in both groups. The systolic and diastolic BP of patients receiving cilazapril was lower compared to baseline for all physical and mental loads. Mean BP reductions over all standardized loads was greater with cilazapril than placebo (-10 vs. -4.3 mm Hg, p < 0.05). These results show that BP is influenced similarly by mental and physical loads, and that behavior [i.e., awake state and non-rapid eye movement and rapid eye movement (NREM and REM) sleep determines BP regulation. Cilazapril is effective in reducing BP in all situations, especially during REM sleep hypertension.
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PMID:Twenty-four-hour blood pressure control: effect of cilazapril on continuous arterial blood pressure during sleep, and physical and mental load in patients with arterial hypertension and sleep apnea. 770 72

Several studies were performed to evaluate the degree of inhibition of angiotensin-converting enzyme (ACE) by an ACE inhibitor by assessing the blood pressure response to a continuous i.v. infusion of increasing doses of angiotensin I in healthy volunteers. We assessed pharmacokinetic and pharmacodynamic interactions of the ACE inhibitor cilazapril and the beta-blocker propranolol in healthy volunteers and patients with essential hypertension. We also evaluated the effect of cilazapril on aortic compliance in hypertension by pulse-wave velocity along the aorta. We showed that single oral doses of cilazapril 4 mg, captopril 25 mg, or enalapril 10 mg shifted the angiotensin I dose-effect curve to the right and determined a pharmacologic half-life of about 4 h for cilazapril. Increasing single oral doses (1.25, 3.75, 10, and 30 mg) of cilazapril reduced diastolic blood pressure dose-dependently and shifted the angiotensin I dose-response curves to the right. The dose representing 50% inhibition of ACE activity (apparent Ki dose) was about 0.6 mg 3 h after cilazapril administration. Cilazapril and propranolol did not exhibit significant pharmacokinetic interaction in healthy volunteers; each drug reduced diastolic and systolic blood pressure by about 7 mm Hg, and this was doubled by the combination. Monotherapy with each drug reduced blood pressure, and combined administration enhanced the antihypertensive effect. The reduction in cardiac output and the increase in total peripheral resistance induced by propranolol were attenuated by the cilazapril-propranolol combination.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Review of studies on the clinical pharmacodynamics of cilazapril. 789 90

Cilazapril, a new angiotensin-converting enzyme (ACE) inhibitor, controls blood pressure (to 90 mm Hg or less) in patients with mild-to-moderate hypertension within 2-3 weeks of initiating treatment (2.5-5.0 mg once daily); this effect was maintained in long-term observations over 1 year. Hemodynamic investigations demonstrated that the antihypertensive action of cilazapril is induced mainly by a decrease of peripheral vascular resistance accompanied by a decrease of pulmonary capillary wedge pressure. Furthermore, cilazapril decreased left ventricular mass index in essential hypertensive patients within 6 months of therapy at doses of 2.5-5.0 mg once daily, thus reversing left ventricular hypertrophy induced by hypertension. In other studies cilazapril was shown to ameliorate glucose tolerance and insulin sensitivity in nondiabetic hypertensive patients, and in hypertensive diabetic patients improvement of renal function was observed. Incidence and severity of side effects caused by cilazapril were comparable to those seen by other ACE inhibitors. Although experimental data provide evidence for vascular, antiatherosclerotic protection by cilazapril, these effects must be proven by long-term prospective studies in humans.
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PMID:Therapeutic experience with cilazapril. 789 97

Endothelium-dependent dilatation of cerebral arterioles is impaired during chronic hypertension. The goal of this study was to determine the effects of an angiotensin converting enzyme inhibitor, cilazapril, on endothelium-dependent dilatation in pial arterioles. Four-month-old Wistar-Kyoto (WKY) rats and stroke-prone spontaneously hypertensive rats (SHRSP) received cilazapril in their drinking water (500 mg/L) for 3 to 6 months. Treatment with cilazapril reduced mean arterial pressure in both WKY rats and SHRSP and had no significant effect on baseline diameter of pial arterioles measured with a cranial window. Responses to bradykinin and A23187, but not to nitroglycerin and adenosine, were impaired in SHRSP. Cilazapril did not affect responses to bradykinin (3 x 10(-7) M) and A23187 (10(-5) M) in WKY rats but significantly increased cerebral vasodilatation in response to bradykinin (52 +/- 4% vs 27 +/- 5%) and A23187 (19 +/- 3% vs 8 +/- 3%) in SHRSP. Cilazapril also tended to increase dilator responses to nitroglycerin and adenosine in SHRSP. In another group of SHRSP, treatment with cilazapril for 4 days produced a moderate reduction in blood pressure and increased cerebral vasodilatation in response to bradykinin, A23187, and adenosine. Topical application of the active form of cilazapril (cilazaprilat) for 40 minutes also increased cerebral vasodilatation in response to bradykinin, A23187, and nitroglycerin in SHRSP. The data indicate that an angiotensin converting enzyme inhibitor enhances cerebral vasodilatation in response to endothelium-dependent agonists in SHRSP and may also increase responses to endothelium-independent agonists.
Hypertension 1993 Aug
PMID:Effects of cilazapril on cerebral vasodilatation in hypertensive rats. 834 Jan 50

Hypertension in animal models and in humans is associated with a decreased vasodilator response to acetylcholine which causes vascular relaxation by release of endothelium-derived relaxing factor from the endothelium. Since lowering of blood pressure, particularly with angiotensin converting enzyme inhibitors, improved the response to acetylcholine we investigated the effects of brachial artery infusions of ascending dosages of acetylcholine on forearm blood flow before and after 5 months of therapy with the angiotensin converting enzyme inhibitor, cilazapril, in 10 patients with mild to moderate primary hypertension. Cilazapril decreased blood pressure from 150.8 +/- 14.4/98.9 +/- 4.3 mmHg during placebo to 138.8 +/- 15.6/88.6 +/- 8.9 mmHg (P < 0.01). Brachial artery acetylcholine infusions increased forearm blood flow from 2.95 +/- 1.5 to a maximum of 22.8 +/- 11.5 ml.min-1.100 ml-1 forearm tissue and decreased forearm vascular resistance from 48.1 +/- 34.1 to 6.9 +/- 6.9 units before cilazapril. This response did not change after cilazapril therapy. Our findings in patients with primary hypertension, therefore, do not support the concept that angiotensin converting enzyme inhibition influences endothelium-dependent vascular relaxation to acetylcholine to a significant degree. Whether this lack of effect on endothelial vasodilator function is specific for the vascular bed chosen for study or whether it represents a fundamental difference between animal models and human hypertension remains an important issue to be clarified.
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PMID:Effects of angiotensin converting enzyme inhibition on endothelial vasodilator function in primary human hypertension. 836 26

We assessed the acute effects of 2.5 mg oral cilazapril on systemic and coronary hemodynamics in seven renovascular hypertensive patients with a chronically overactive renin-angiotensin system (RAS), but with no electrocardiographic or echocardiographic signs of left ventricular hypertrophy. Cilazapril resulted in a significant decrease in mean arterial pressure and coronary vascular resistance, together with a prolonged increase in coronary sinus blood flow (CSBF). Post-cilazapril handgrip resulted in larger increases in CSBF in response to a given increase in myocardial oxygen requirements. It is concluded that the chronic activation of the RAS exerts an adverse influence on the control mechanisms of CSBF and that converting enzyme inhibition reverses the effects of angiotensin II on coronary hemodynamics. Converting enzyme inhibitors may have a cardioprotective role in renovascular hypertension.
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PMID:Coronary blood flow in renovascular hypertension. 848 57

Contrasting information has been reported concerning the course of renal function in NIDDM with hypertension alone or in association with renal damage. The aim of the present study was to elucidate the course of the glomerular filtration rate (GFR) in hypertensive NIDDM patients during antihypertensive therapy. Furthermore, we compared the effects of ACE inhibitors (cilazapril, Inibace, Roche, Milan, Italy) and Ca(2+)-channel blockers (amlodipine, Norvasc, Pfizer, Rome, Italy). Of the hypertensive NIDDM patients attending the outpatient's clinic of the internal medicine departments of the University of Padova and Sassari, 44 participated in the present study. Of these patients, 26 were normoalbuminuric and 18 microalbuminuric. They were randomly treated with either cilazapril or amlodipine. The target of antihypertensive treatment was a value < 140 mmHg for systolic and 85 mmHg for diastolic blood pressure (BP). Microalbuminuria was defined as an albumin excretion rate (AER) between 20 and 200 micrograms/min. GFR was measured by plasma clearance of 51Cr-labeled EDTA at baseline and every 6-12 months during a 3-year follow-up interval. A significant decrease was observed in the values of GFR, AER, and systolic and diastolic BP in normoalbuminuric and microalbuminuric patients during antihypertensive therapy. The GFR fall in the overall population of NIDDM patients was significantly and inversely related to the decrease of mean BP (diastolic + 1/3 pulse pressure) (r = -0.80, P < 0.0001) but not to that of HbA1c, triglycerides, and BMI. The GFR decline (mean +/- SE) per year in the normoalbuminuric patient was 2.03 +/- 0.66 ml.min-1 x 1.73 m-2 (95% CI 0.92-3.17) during cilazapril and 2.01 +/- 0.71 ml.min-1 x 1.73 m-2 (95% CI 0.82-3.11) during amlodipine therapy. The GFR decline per year in the microalbuminuric patient was 2.15 +/- 0.69 ml.min-1 x 1.73 m-2 (95% CI 0.86-3.89) during cilazapril and 2.33 +/- 0.83 ml.min-1 x 1.73 m-2 per year (95% CI 1.03-3.67) during amlodipine therapy. Cilazapril and amlodipine lowered AER to a similar extent in normoalbuminuric and microalbuminuric patients. No significant changes were observed concerning other clinical and biochemical features between the two antihypertensive therapies and particularly HbA1c, BMI, triglycerides, and cholesterol plasma values. These results support the tenet that arterial hypertension plays a pivotal role in contributing to renal damage in NIDDM, even when AER is normal. However, the degree of BP control, with both cilazapril and amlodipine, can successfully delay the slope of GFR decline in hypertensive NIDDM patients with or without incipient nephropathy.
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PMID:Effects of cilazapril and amlodipine on kidney function in hypertensive NIDDM patients. 854 68

Hypertension is associated with an altered design of resistance vessels and decreased endothelium-dependent vasodilator response to acetylcholine. A role of angiotensin II in both defects is suggested by animal experiments in which angiotensin-converting enzyme inhibition reverted structural and functional changes. We investigated the effects of 20 weeks of therapy with the angiotensin-converting enzyme inhibitor cilazapril (5 mg twice daily) on the endothelium-dependent response to brachial artery infusions of acetylcholine and the endothelium-independent vascular relaxation after sodium nitroprusside in 22 subjects with mild to moderate essential hypertension. In addition, we measured minimal forearm vascular resistance (ratio of mean arterial pressure and forearm blood flow after heating, ischemia, and ischemic exercise) as an indirect estimate of vascular structure. Cilazapril decreased blood pressure (151 +/- 14/99 +/- 7 mm Hg during placebo to 138 +/- 17/89 +/- 8 mm Hg after cilazapril treatment, P<.01) and baseline (42.2 +/- 12.6 to 37.1 +/- 10.6 U, P<.05) and minimal (3.0 +/- 1.1 to 2.4 +/- 0.7 U, 15.9 +/- 20.2%; P<.05) forearm vascular resistances. The change in minimal forearm vascular resistance was unrelated to age, duration of hypertension, or changes in blood pressure. Sodium nitroprusside increased forearm blood flow from 2.6 +/- 1.0 to 11.4 +/- 5.9 mL/min per 100 mL and acetylcholine to 21.5 +/- 17.8. Both responses did not change after cilazapril. The data provide indirect evidence that cilazapril therapy may improve vascular structure in human hypertension. The lack of relationship between vascular and blood pressure changes would be compatible with experimental evidence supporting a role for angiotensin II in the development and regression of vascular changes, but this needs further study. Therapy with cilazapril for 20 weeks, like other antihypertensive therapy, does not seem to influence endothelial vasodilator function in humans to a significant degree.
Hypertension 1996 Mar
PMID:Effects of cilazapril on vascular structure and function in essential hypertension. 869 40


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