Monopril scientific update |
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Chin J Integr Med. 2006 Sep;12(3):166-70.
Cheng WL, Ke YN, Shi ZX, Wang Y, Chen L, Ju G, Fan SY.
Department of National Integrative Medicine Center for Cardiovascular Diseases, China-Japan Friendship Hospital, Beijing (100029).
Clinical study on effect of garlicin in stabilizing the carotid artery atherosclerotic plaque in patients with primary hypertension and coronary artery disease.
OBJECTIVE: To investigate the effect of garlicin in treating carotid artery atherosclerotic plaque (CAAP) in patients with primary hypertension and coronary heart disease (PHT-CHD). METHODS: Seventy-nine patients with PHT-CHD were randomly divided into the treated group (39 patients) treated with garlicin and fosinopril and the control group (40 patients) treated with fosinopril alone. The change of CAAP was evaluated by high frequency ultrasonic examination every six months, and the changes of intercellular adhesion molecule-1 (ICAM-1) and high sensitive C-reactive protein (hs-CRP) were measured by ELISA, with the observation proceeding for 52 weeks totally. RESULTS: By the end of the experiment, the number of complex plaques, Crouse integrals, intima-media thickness, serum ICAM-1 and hs-CRP were significantly lower in the treated group than those in the control group with significant difference (P < 0.05). CONCLUSION: Garlicin could stabilize CAAP to a certain extent and shows a definite vascular protective effect in patients with PHT-CHD.
Pharmacol Res. 2004 Aug;50(2):131-6.
el-Batran SA, el-Shenawy SM, Nofal SM, Abdel-Salam OM, Arbid MS.
Department of Pharmacology, National Research Center, Doki, Cairo, Egypt.
Studies on the glycemic and lipidemic effect of monopril and losartan in normal and diabetic rats.
The effects of the angiotensin-converting enzyme (ACE) inhibitor monopril and the angiotensin II receptor blocker losartan on serum glucose, protein levels and some serum lipid components were compared in normal and diabetic rats receiving oral antidiabetic drugs 'repaglinide or gliclazide'. The two antihypertensive agents, when administered concurrently with oral hypoglycemic agents 'repaglinide or gliclazide' in normal and diabetic rats exerted a significant hypoglycemic effect. Serum protein levels were mainly unaffected by the two antihypertensive drugs. Monopril and losartan exhibit a hypolipidemic effect in normal and diabetic rats when administered in combination with oral hypoglycemic agents 'gliclazide or repaglinide'. Monopril or losartan when used alone exerted insignificant effect in high density lipoprotein (HDL) in normal rats, while in combination with gliclazide or repaglinide caused a significant increase in HDL in normal rats. Concomitantly, monopril or losartan, when administered alone or in combination with repaglinide or gliclazide in diabetic rats exerted a significant increase in serum HDL. On the other hand, all the investigated drugs showed a significant decrease in serum low density lipoprotein (LDL) in normal and diabetic rats. Copyright 2004 Elsevier Ltd.
Stroke. 2005 Mar;36(3):649-53. Epub 2005 Feb 03.
Asselbergs FW, van Roon AM, Hillege HL, de Jong PE, Gans RO, Smit AJ, van Gilst WH
Department of Clinical Pharmacology, University of Groningen, Antonius Deusinglaan 1, 9713 AV, Groningen, The Netherlands.
Effects of fosinopril and pravastatin on carotid intima-media thickness in subjects with increased albuminuria.
BACKGROUND AND PURPOSE: Elevated urinary albumin excretion (UAE) is associated with an increased carotid intima-media thickness (IMT). Because angiotensin-converting enzyme inhibitors as well as statins have been shown to lower UAE and the progression of IMT, we assessed the effects of fosinopril and pravastatin on carotid IMT in subjects with an increased UAE (15 to 300 mg/24 h). METHODS: IMT was measured at the posterior wall of the left common carotid artery using radio-frequency signal analysis obtained by M-mode ultrasonography. 642 subjects were double-blind randomized to fosinopril 20 mg or matching placebo and to pravastatin 40 mg or matching placebo and were available for intention-to-treat analysis. RESULTS: Mean age was 51+/-11 years, 65% were male, the median UAE was 22.5 (15.5 to 40.8) mg/24 h, and the mean IMT at baseline was 0.77+/-0.18 mm. The overall progression rate of IMT in 4 years was 0.037+/-0.006 mm. No significant difference in IMT progression was found between fosinopril, pravastatin, or matching placebo. IMT after 4 years was predicted by IMT at baseline, age, gender, pulse pressure, and low-density lipoprotein cholesterol levels. Furthermore, a higher incidence of clinical events was observed in subjects with an IMT >1 mm after a mean follow-up of 46+/-7 months (hazard ratio, 3.13; 95% confidence interval, 1.59 to 6.16; P=0.001). CONCLUSIONS: In subjects with an increased UAE, treatment with fosinopril and pravastatin showed no significant effect on carotid IMT. Furthermore, an IMT <1 mm at baseline is an important indicator for event-free survival.
Nephrol Dial Transplant. 2005 May;20(5):892-901. Epub 2005 Mar 8.
Zhang W, Chen X, Shi S, Wei R, Wang J, Yamanaka N, Hong Q.
Department of Nephrology, General Hospital of PLA, Beijing 28 Fuxing Road, 100853, P.R. China.
Expression and activation of STAT3 in chronic proliferative immune complex glomerulonephritis and the effect of fosinopril.
BACKGROUND: Signal transducers and activators of transcription (STATs) are cytoplasmic proteins that are activated in response to stimulation from various cytokines. Among these, STAT3 is an important member that has been implicated in the inflammatory proliferation of cells. We hypothesized that STAT3 may be activated in kidneys of rats having modified chronic immune complex glomerulonephritis, and that angiotensin-converting enzyme (ACE) inhibition with fosinopril may prevent the activation of STAT3 and subsequent upregulation of tissue inhibitor of metalloproteinase-1 (TIMP-1), which are effects that may explain the therapeutic effects of fosinopril on nephritis. METHODS: Fifty-one Wistar rats were randomly divided into three groups that included a control group, a model group and a fosinopril group. Bovine serum albumin (BSA) nephritis was induced by subcutaneous immunization and daily intraperitoneal (i.p.) administration of BSA. To accentuate the nephritis, we performed uni-nephrectomy and gave 100 microg of lipopolysaccharide (LPS) as an i.p. injection. Macrophage infiltration (ED-1) was assessed with immunohistochemistry. The expression and activation of STAT3 and the expression of TIMP-1, one of the STAT3 downstream genes, were observed in renal tissues of rats by means of immunohistochemistry, electrophoretic mobility shift assay (EMSA), western blot and northern blot. The relationships between STAT3 phosphorylation, 24 h urinary protein excretion and TIMP-1 expression were also analysed. RESULTS: Northern blot showed that the mRNA expression of both STAT3 and TIMP-1 was significantly increased in kidneys from the model group, but significantly decreased in the fosinopril group (P<0.05). Western blot analysis revealed similar increases in the expression of STAT3, phospho-STAT3 (p-STAT3) and TIMP-1 in the model group. Analysis of immunohistochemistry showed that STAT3 and p-STAT3 were expressed in very few cells of normal rats, that expression was strong in model rats and that this increased expression was attenuated in the fosinopril group (P<0.05). The expression of p-STAT3 in glomeruli was positively correlated with 24 h proteinuria as well as with glomerular TIMP-1 expression. Double staining showed that some ED-1-positive cells also contained p-STAT3-positive staining. CONCLUSIONS: The present study showed that STAT3 is expressed and activated in kidneys of rats with modified immune complex glomerulonephritis. These rats also had increased ED-1-positive cells, with some cells showing simultaneous expression of p-STAT3 and ED-1, which may contribute to glomerular inflammatory proliferation and extracellular matrix accumulation. Finally, fosinopril downregulated STAT3 activation and ED-1 influx, which are effects that may attenuate renal damage in this model.
Int J Clin Pract. 2005 Mar;59(3):306-10.
Bilge AK, Atilgan D, Tukek T, Ozcan M, Ozben B, Koylan N, Meric M.
Department of Cardiology, Istanbul University, 34390 Capa, Istanbul, Turkey.
Effects of amlodipine and fosinopril on heart rate variability and left ventricular mass in mild-to-moderate essential hypertension.
The differences between long-acting dihydropyridines and angiotensin-converting enzyme inhibitors with regard to their long-term effects on 24-h heart rate variability (HRV) and left ventricular (LV) mass are less clear in mild-to-moderate essential hypertension. We studied the long-term effects of amlodipine and fosinopril on 24-h HRV and LV mass in mild-to-moderate essential hypertension. In this study, 27 patients with never treated mild-to-moderate essential hypertension were randomised to receive either amlodipine or fosinopril once daily as monotherapy. At baseline and at the end of the third and sixth months, each of the patients underwent 24-h HRV and ambulatory systolic (SBP) and diastolic (DBP) blood pressure analysis. LV mass index was calculated from echocardiographic examination at baseline and at the end of the sixth month. In amlodipine group (n = 14), 24-h SBP/DBP (mmHg) decreased from 144 +/- 8/94 +/- 4 to 128 +/- 6/83 +/- 3 at the end of the third month and to 125 +/- 5/81 +/- 2 at the end of the sixth month (p < 0.0001). In fosinopril group (n = 13), the respective changes were 143 +/- 9/97 +/- 7, 132 +/- 6/87 +/- 5 and 127 +/- 6/82 +/- 3 (p < 0.0001). At the end of the sixth month, LV mass index (g/m(2)) decreased from 122 +/- 26 to 105 +/- 21 in amlodipine group (p < 0.0001) and from 118 +/- 23 to 101 +/- 14 in fosinopril group (p < 0.0001). There were no significant changes in HRV parameters in both the groups. It was concluded that both drugs caused significant decrease in SBP and DBP, and LV mass in patients with mild-to-moderate essential hypertension did not have significant long-term effects of either amlodipine or fosinopril on 24-h HRV parameters reflecting sympathetic or parasympathetic activity in these patients.
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Drug category:Hypotensive agents
 Monopril scientific update
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