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Vnitr Lek. 1999 Dec;45(12):696-702.
[Pharmacotherapy in patients with ischemic heart disease and diabetes mellitus in 1998 in the Czech Republic]

[Article in Czech]

Widimsky J, Juran F, Leisser J, Vanek P, Lanska V.

Klinika kardiologie IPVZ, Praha.

The state of pharmacotherapy in the Czech Republic in 1998 was analysed in a group of 548 patients with coronary heart disease and diabetes mellitus. 83.0% of the group were treated by antiplatelet drugs, mostly ASA (with the most frequent dose being 100 mg). 7.3% of the patients were treated by anticoagulation treatment. Beta-blocking agents were used in 56.9% of the group (most frequently metoprolol and atenolol). The optimal dose of metoprolol, 100 mg b.i.d., was used in only 12.4% of the patients treated by metoprolol. Older patients and patients with left ventricular systolic dysfunction were treated significantly less frequently than younger patients or patients without left ventricular systolic dysfunction. ACE inhibitors were used in 52.2% of the patients. The optimal daily target dosages of captopril 100-150 mg were used in only 6% of patients treated by captopril. The optimal target daily dosages of enalapril were used in only 35.1% of patients treated by enalapril. 65% of patients with left ventricular systolic dysfunction were treated by ACE inhibitors. Calcium-channel blockers were used in 24.6% of the patients. However, in 20.1% of patients treated by calcium-channel blockers, shortacting or inadequately retarded nifedipine was used. 69.8% of the patients had total cholesterol values higher than 5.2 mmol/l, 18.1% higher than 6.2 mmol/l and 13.5% of patients had total cholesterol values higher than 7.0 mmol/l. 34.3% of the group were treated by hypolipidemic drugs (most frequently fenofibrate). Statins were used by 45.5% of patients treated by hypolipidemic drugs. When compared to our analysis of pharmacologic treatment in patients after myocardial infarction, performed in 1995, ACE inhibitors and hypolipidemic treatment are used more frequently. However, in spite of this improvement, only about 15% of patients with CHD are treated by statins. Furthermore, 35% of patients with left ventricular systolic dysfunction due to CHD are not treated by ACE inhibitors. Elderly patients with CHD and diabetes mellitus or patients with left ventricular systolic dysfunction due to CHD are less frequently treated than younger patients or those with normal left ventricular systolic function despite the fact that patients at highest risk benefit most from treatment with beta-blocking agents. Also unsatisfactory is the use of not retarded or inadequately retarded nifedipine although data show its use may increase total mortality in CHD patients. By contrast, use of antiplatelet therapy is satisfactory.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10951843&dopt=Abstract

Scand J Urol Nephrol Suppl. 1984;79:23-7.
Differing effects of two angiotensin converting enzyme inhibitors, captopril and CI-906, on diuresis and the urinary excretion of kallikrein and prostaglandins in spontaneously hypertensive rats.

Saynavalammi P, Porsti I, Nurmi AK, Seppala E, Laitinen LA, Manninen V, Ylitalo P, Vapaatalo H.

The effects of two angiotensin I converting enzyme inhibitors on the kallikrein-kinin system and prostanoids were studied in spontaneously hypertensive rats. The doses of captopril were 20, 50 and 100 mg/kg X day given twice daily, and those of CI-906 20 and 40 mg/kg once daily. Both drugs were equally effective in reducing the systolic blood pressure. Captopril increased urine volume dose-dependently (up to 3-fold with the largest dose). Only the larger dose of CI-906 was slightly diuretic. Captopril decreased the 24-h urinary excretion of kallikrein, while the excretion of the prostacyclin metabolite 6-keto-PGF1 alpha was increased markedly and that of T X B2 to a lesser extent. CI-906 had no effect on the 24-h urinary excretion of kallikrein, 6-keto-PGF1 alpha and T X B2. Both drugs tended to reduce PGE2 excretion. Captopril and CI-906 did not alter plasma kininogen levels. The marked renal effects of captopril may be caused by a strong local inhibition of converting enzyme in the kidneys. Captopril is mainly excreted unchanged in urine, and it is secreted actively by the proximal tubular cells. CI-906 is eliminated predominantly by biliary excretion. It is also possible that direct stimulation of prostacyclin formation by captopril may be involved in the diuretic action of the drug. However, as it was shown with CI-906, the increase in urine flow and the associated changes in urinary kallikrein and prostanoids are not necessary for the antihypertensive effect caused by the inhibition of converting enzyme.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=6089314&dopt=Abstract

J Hypertens. 2000 Aug;18(8):1051-6.
Insulin and insulin-like growth factor-I promotes angiotensinogen production and growth in vascular smooth muscle cells.

Kamide K, Hori MT, Zhu JH, Takagawa Y, Barrett JD, Eggena P, Tuck ML.

Division of Endocrinology, Department of Veterans Affairs, Greater Los Angeles Health Care System, Sepulveda, California 91343, USA.

BACKGROUND: Circulating insulin and insulin-like growth factor-I (IGF-I) levels are increased in patients with hypertension and insulin resistance. Since both hormones are known to have cell growth-promoting effects, they may contribute to the progression of vascular hypertrophy in patients with insulin resistance. Insulin-mediated activation of the vascular renin-angiotensin system (RAS) stimulates growth in cultured rat vascular smooth muscle cells (VSMC). OBJECTIVE: In order to evaluate the role of IGF-I-mediated activation of components of the tissue RAS, we examined the effect of IGF-I receptor stimulation on cell proliferation, and production of angiotensinogen in cultured VSMC. STUDY DESIGN: Aortic VSMC were derived from male Sprague-Dawley rats. IGF-I and insulin-mediated DNA synthesis were estimated by 3H-thymidine uptake (3H-TdR) with or without the angiotensin I converting enzyme inhibitor, captopril. Moreover, angiotensinogen released by the cells to the culture medium was determined by radioimmunoassay with or without the anti-IGF-I receptor antibody alphaIR3 or captopril. RESULTS: Both IGF-I and insulin increased 3H-TdR uptake by cultured rat VSMC (P < 0.05). Captopril blocked IGF-I and insulin-mediated 3H-TdR uptake (-34.4 +/- 1.9% and -32.7 +/- 1.8%, P < 0.05, respectively). IGF-I increased the angiotensinogen level in the medium by 30.6 +/- 2.9% (P < 0.01). Insulin also stimulated angiotensinogen synthesis by 26.3 +/- 2.2% (P < 0.01). Captopril and alphaIR3 significantly suppressed angiotensinogen production stimulated by both IGF-I and insulin. CONCLUSIONS: These results indicate that IGF-I as well as insulin stimulates angiotensinogen production and growth in VSMC. Thus, both hormones may independently play a role in progression of the vascular hypertrophy and atherosclerosis in patients with hypertension and insulin resistance through activation of the tissue RAS.

online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10953996&dopt=Abstract

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