Drugs online research references
Clin Sci (Lond). 1999 Aug;97(2):233-7.
Ramipril prevents basal arterial constriction and enhanced myogenic tone in the femoral artery in mildly uraemic normotensive rats.
Savage T, McMahon AC, Mullen A, Tribe RM, Yaqoob MM.
Anthony Raine Research Laboratories, St. Bartholomews Hospital, Dominion House, 59 Bartholomew Close, West Smithfield, London EC1A 7BE, U.K.
Some aspects of vascular reactivity are altered in mild experimental uraemia, as shown by increased myogenic tone and a reduced lumen diameter in the femoral artery. This study was conducted to investigate the prevention of these uraemia-induced vascular abnormalities by the angiotensin-converting enzyme inhibitor (ACE-I) Ramipril. Ten male Wistar rats were rendered uraemic (U) by 5/6th nephrectomy, and 10 control (C) rats were concurrently sham-operated. After 4 weeks, both groups were given daily subcutaneous injections of 3 microg of Ramipril for a further 4 weeks. Tail-cuff systolic blood pressure was then recorded and the rat was killed. Isolated femoral arteries were mounted on a pressure myograph and pressurized at 40 mmHg for baseline measurements of the lumen internal diameter. Myogenic tone was then assessed over a range of intravascular pressures from 40 to 160 mmHg. Biochemically, serum urea and creatinine were significantly higher in the uraemic (U) group [urea: U, 23+/-3 mmol/l; C, 6+/-1 mmol/l (P<0.001); creatinine: U, 147+/-17 mmol/l, C, 72+/-11 mmol/l (P<0.01)]. Systolic blood pressure was the same in both groups (U, 127+/-7 mmHg; C, 127+/-3 mmHg). The mean baseline internal diameter was the same in both groups (U, 756+/-22 microm; C, 721+/-34 microm, not significant), as was mean myogenic tone (U, 4.7+/-1%; C, 3.4+/-1%). In conclusion, there were no differences in baseline lumen diameter or myogenic tone in uraemic compared with control femoral arteries of rats treated with Ramipril, which suggests that Ramipril may prevent the development of elevated myogenic tone and decreased lumen diameter previously observed in this model of uraemia. These results suggest that these specific vascular abnormalities in uraemia may be mediated by renin or bradykinin, or by the direct action of angiotensin II on vascular smooth muscle.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=10409479&dopt=Abstract
kms.mhn.de
Patients with end-stage renal disease die from cardiovascular disease at a much younger age than people in the general population do. Here, we review the evidence linking early renal insufficiency (ERI) to an increased cardiovascular risk. A number of cardiovascular risk factors become prevalent with ERI, including night-time hypertension, increase in serum levels of lipoprotein (a), homocysteine and asymmetric dimethyl-arginine, and insulin resistance. Also, an epidemiologic association between coronary artery disease (CAD) and nephrosclerosis, a frequent cause of ERI in the elderly, is documented. In the middle-aged, general population ERI, found in 8% of women and 9% of men, was not associated with cardiovascular disease. However, in a representative sample of middle-aged British men the risk of stroke was 60% higher for the subgroup of individuals with ERI. In people at high cardiovascular risk (mostly CAD), the Heart Outcomes Prevention Evaluation (HOPE) study found a 2-fold (unadjusted) or 1.4-fold (adjusted) higher incidence of cardiovascular outcomes with ERI. The incidence of primary outcome increased with the level of serum creatinine. At least four studies have determined the cardiovascular risk associated with ERI in hypertension. In Hypertension Detection and Follow-up Program, as in HOPE, cardiovascular mortality increased with higher serum creatinine levels (5-fold difference in cardiovascular mortality between the lowest and the highest creatinine strata). In patients with hypertension with low risk, the Hypertension Optimal Treatment and a small Italian trial found about a doubling in cardiovascular outcomes in ERI. However, in the Multiple Risk Factor Intervention Trial, not baseline serum creatinine level, but its increase on follow-up predicted future cardiovascular disease. These observational data suggest that ERI, independent of etiology, is a strong predictor of cardiovascular disease, present in 10% of a population at low, and up to 30% at high, cardiovascular risk. No prospective therapeutic trials aimed at reducing the cardiovascular burden in individuals with ERI are available. Subgroup analyses of the HOPE study indicate that ACE inhibition with ramipril is beneficial without an increased risk of adverse effects like acute renal failure or hyperkalemia. Thus the frequent practice of withholding ACE inhibitors from patients with mild renal insufficiency is unwarranted, especially since this identifies a group at high risk who appears to benefit most from treatment. In addition, there is evidence that ACE inhibitors improve renal outcomes in renal insufficiency. Prospective studies should test the predictive power of ERI for cardiovascular disease and therapeutic options.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14727978&dopt=Abstract [PubMed - in process]
Am J Cardiovasc Drugs. 2003;3(5):351-60.
ACE Inhibition with Moexipril : A Review of Potential Effects Beyond Blood Pressure Control.
Pines A, Fisman EZ.
Department of Medicine "T", Ichilov Hospital, affiliated to the Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
ACE inhibitors induce metabolic changes and exert cardioprotective and vasoprotective properties, some of which cannot be attributed to their antihypertensive effect per se. Moexipril is an ACE inhibitor with a lipophilicity in the same range as quinapril, benazepril or ramipril, and so can readily penetrate lipid membranes and thus target tissue ACE in addition to plasma ACE. Evidence from animal studies shows similar and significant (p < 0.05) reductions in tissue ACE activity for moexipril and quinapril.Moexipril may improve endothelial dysfunction; moexiprilat and ramiprilat have demonstrated greater activity than captopril, enalaprilat and quinaprilat in isolated endothelium-denuded segments of the rabbit jugular vein where bradykinin elicits a constrictor response, mediated by activation of the bradykinin B(2) receptor.ACE inhibitors, including moexipril, may exert neuroprotective effects. Moexipril promoted neuronal survival in vitro and it is thought that this neuroprotective effect is due to free radical scavenging properties of the drug. ACE inhibitors can also decrease progression of renal insufficiency in patients with various underlying renal diseases. Moexipril may also have a renoprotective effect as it increased the ultrafiltration coefficient and normalized urinary protein excretion in rat models. Preclinical studies indicate that the renin-angiotensin-aldosterone system may play a role in the regulation of bone resorption and moexipril had no adverse effects on bone metabolism in animal models and the drug did not hamper the osteoprotective effects of estrogen.Reduction in left ventricular mass with moexipril in patients with hypertension was similar in magnitude to the effect of other ACE inhibitors. When investigated in hypertensive patients with an elevated cardiovascular risk, moexipril increased arterial distensibility and demonstrated antioxidative properties in addition to efficiently controlling blood pressure. Moexipril does not adversely affect serum levels of uric acid, lipids, blood glucose levels and plasma insulin levels and can be co-administered with hormone replacement therapy. Moreover, quality-of-life data suggest favorable effects of moexipril treatment in a patient population at high cardiovascular risk.
online pharmacy ref source: www.ncbi.nlm.nih.gov/entrez/query.fcgi?cmd=Retrieve&db=PubMed&list_uids=14728069&dopt=Abstract [PubMed - in process]
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