Drugs online research references
Bratisl Lek Listy. 1997 Dec;98(12):687-94.
[Bioenergetics of liver mitochondria after administration of ramipril in experimental diabetes mellitus]
[Article in Slovak]
Ulicna O, Cizova M, Kolesar P, Volkovova K, Cibulova L, Carsky J, Ondrejka P.
Farmakobiochemicke laboratorium III. internej kliniky Lekarskej fakulty Univerzity Komenskeho v Bratislave, Slovakia.
BACKGROUND: Diabetes mellitus represents an intense metabolic strain for the liver. Inhibitors of angiotensin-converting enzymes (ACEI) are drugs of choice in the therapy of hypertension in coincidence with diabetes mellitus. The effect of ACEI is complex. The attention is drawn to the study of metabolic effects of ACEI. OBJECTIVES: The aim of the study was to investigate whether the administration of ramipril affects the levels of glycated hemoglobin and fructoseamine in the blood of rats with insulin-dependent diabetes mellitus (IDDM), and whether bioenergetics of mitochondria in the liver undergo changes. METHODS: In our experiments, we used rats of the Wistar strain. The control group was composed of healthy animals. The experimental groups were formed by rats with IDDM evoked by streptozotocine (45 mg/kg) and rats with IDDM + ramipril (10 mg/KG). Both, insulin MONO-ID in the doses of 6 U/kg administered subcutaneously, and water solution of ramipril administered by gastric probe were applied for the period of 8 weeks. We have assessed blood levels of glucose, glycated hemoglobin, fructoseamine and the concentration of cholesterol and triacylglycerols have been assessed also in the liver. Oxidative phosphorylation in mitochondria of the liver were measured polarographically. RESULTS: In the group with IDDM + ramipril, the glycated haemoglobin (M 6.85 CI 5.7-7.0%) and fructoseamine (M 1.45 CI 1.2-1.6 mmol/l) have significantly dropped in comparison with the group with IDDM glycated haemoglobin (M 8.8 7.7-10.7%) and fructoseamine (M 2.04 CI 1.69-2.4 mmol/l). Ramipril did not affect the concentration of cholesterol and triacylglycerols in the blood and liver in rats with IDDM. Ramipril has positively affected oxidative phosphorylation in mitochondria of the liver in coincidence with IDDM. The group with IDDM + ramipril has yielded an increase in the velocity of oxygen consumption in coincidence with stimulated breathing with ADP, the state 3 (M 107.97 CI 96.78-134.51 n AtO/mg of proteins/min.) and phosphorylation velocity (M 232.67 CI 209.38-284.97 nmolATP/protein/min) in contrast to the group with IDDM: the state 3 (M 76.71 CI 66.81-85.99 nAtO/mg of proteins/min and the velocity of phosphorylation (M 161.84 CI 143.55-189.99 nmol ATP/mg of proteins/min) in coincidence with substrate glutamate. A similar trend is present also in coincidence with FAD succinate substrate. CONCLUSIONS: After the administration of ramipril to rats with IDDM, the indicators have improved, and they express the rate of compensation of diabetes mellitus. An increased capacity of the respiratory chain and an increased origin of energy in mitochondria in the livers of rats with IDDM after administration of ramipril indicates an improvement in the metabolic capacity of the liver. (Tab. 4. Ref. 47.)
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=9525068&dopt=Abstract
Am J Physiol. 1993 May;264(5 Pt 2):H1493-7.
Effect of angiotensin-converting-enzyme inhibition on bradykinin metabolism by vascular endothelial cells.
Grafe M, Bossaller C, Graf K, Auch-Schwelk W, Baumgarten CR, Hildebrandt A, Fleck E.
Department of Cardiology, German Heart Institute, Berlin.
The degradation of bradykinin by angiotensin-converting-enzyme (ACE) activity in cultured human endothelial cells was studied by direct measurement of bradykinin and by its effect on the release of endothelium-derived relaxing factors. The half-life of exogenous bradykinin (10,000 pg/ml) was calculated from the decay of the bradykinin concentration as 46 +/- 2 min in cell monolayers, 133 +/- 15 min in conditioned medium, and 24 +/- 2 min in homogenates. Most of the bradykinin-degrading activity in cell monolayers could be inhibited in a concentration-dependent manner by the ACE inhibitors lisinopril, ramiprilat, and captopril. Bradykinin-degrading activity was released into the culture medium containing one-fourth of the bradykinin-degrading activity found in the presence of cell monolayers. In cell homogenates higher unspecific bradykinin-degrading activities were present. The functional consequence of bradykinin degradation was demonstrated by the potentiating effect of ramiprilat on the generation of endothelium-derived relaxing factors nitric oxide and prostacyclin from endothelial cells. The study supports the concept of increased vasodilatory effects of bradykinin during ACE inhibition.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=8388656&dopt=Abstract
Am J Hypertens. 1999 Mar;12(3):311-4.
Central vasopressin is modulated by chronic blockade of the renin-angiotensin system in experimental left ventricular hypertrophy.
Muders F, Elsner D, Schunkert H, Riegger GA, Palkovits M.
Klinik und Poliklinik fur Innere Medizin II, University of Regensburg, Germany.
We studied the interaction of the central renin-angiotensin system (RAS) and vasopressin system in rats with left ventricular hypertrophy (LVH) due to aortic banding. In these animals plasma vasopressin is elevated and vasopressin content is increased in specific brain areas. Chronic blockade of the RAS by angiotensin-converting enzyme (ACE) inhibition (ramipril) and AT1 receptor antagonism (losartan) significantly attenuated circulating and central vasopressin in rats with LVH. Given the antidiuretic, vasoconstrictive, and growth-promoting effects, vasopressin may participate in the cardiovascular alterations in LVH. Blockade of the RAS strongly ameliorates central and peripheral-vasopressin. Therefore, central modulatory effects on vasopressin might contribute to the therapeutic efficacy of ACE inhibitors and AT1 antagonists.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10192235&dopt=Abstract
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