Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: EC:3.4.15.1 (ACE)
 18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Vasodilator therapy has been utilized for the treatment of congestive heart failure in the last 20 years. These drugs contribute to increase cardiac output, decrease peripheral vascular resistance and favour venous dilatation. Recent multicenter trials have addressed the issue of the impact of vasodilator therapy upon survival. Thus, the VHEFT-I and Consensus studies have shown that both the combination of nitrates and hydralazine and ACF inhibitors improve life expectancy in patients with moderate and severe heart failure. Moreover, the SOLVD study showed that ACE inhibitors improve survival and reduce cardiac events in patients with mild heart failure and depressed myocardial function at the end of 2 years of follow-up. The VHEFT II trial compared the effects of the nitrate-hydralazine combination versus ACE inhibitors upon the clinical course of patients with moderate heart failure. This last trial showed that although nitrates and hydralazine exerted a slightly better benefit upon exercise tolerance and left ventricular ejection fraction, patients that were treated with ACE inhibitors had a significantly reduced mortality. Differences in mortality when both groups of vasodilators drugs were compared were due to reduction of arrhythmias and sudden death. It is likely that this greater benefit obtained with ACE inhibitors when compared to nitrates and hydralazine in heart failure might be due to their favourable effects upon the abnormal neurohormonal activation observed in this syndrome. Thus ACE inhibitors have turned out to be one of the cornerstones in the treatment of congestive heart failure.
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PMID:[Vasodilator agents in chronic heart failure: which is the best option?]. 823 72

Recent studies have shown that increased intake of dietary sodium chloride produces blood pressure-independent increase in cardiac and renal mass even in young normotensive rats. With advancing age the harmful cardiovascular effects of increased dietary sodium are not so well known. In the present study the influence of advancing age on the cardiovascular effects of increased intake of sodium (control diet, 0.3% and high-sodium diet, 2.6% sodium in the chow) were examined in young and aged (3 and 18 months old, respectively, at the beginning of the experiment) male normotensive Wistar rats in a six-week study. Moreover, the potential role of renin-angiotensin system in ageing during normal and a high-sodium intake was studied using a pharmacological tool, angiotensin converting enzyme (ACE) inhibitor ramipril. Ageing did not significantly modify basal systolic blood pressure measured by the tail cuff method. A high intake of sodium chloride increased blood pressure significantly only in aged rats, while in young rats it increased renal weight. Left ventricular weight was not affected by high-sodium diet in either age group. The ACE inhibition during control diet lowered blood pressure and decreased left ventricular weight in young rats only and these effects were completely blocked by a high-sodium diet. The maximal vascular contraction force of mesenteric arterial rings to noradrenaline was decreased with ageing while endothelium-dependent and -independent relaxation responses were unaltered with ageing. The sensitivity to sodium nitroprusside was impaired by the high-sodium diet in young rats. In both age groups the urinary excretion of calcium was increased during the high-sodium diet. In conclusion, the increased intake of sodium produced different changes in cardiovascular function in normotensive rats depending on age. With advancing age, the sensitivity to sodium-induced increase in blood pressure was increased. In aged rats a high intake of dietary sodium elevated blood pressure, while in young rats it increased renal mass without increase in blood pressure. In both age groups sodium did not affect left ventricular hypertrophy. Both high-sodium intake and ageing attenuated or even abolished the cardiovascular effects of ACF inhibition.
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PMID:Influence of age on cardiovascular effects of increased dietary sodium and angiotensin-converting enzyme inhibition in normotensive Wistar rats. 930 61

The objective of the present study was to investigate the association between diabetes mellitus and colorectal carcinogenesis as well as the possible mechanism involved in this interaction. Diabetes rat models were induced with a low dose of STZ followed by a low dose of DMH to induce colorectal cancer. The formation of ACF in the colon and the incidence, number and size of tumors were measured. The activity of glycolytic enzymes in colonic tissues was also measured. The results demonstrated that both the total number of ACF and the number of foci that contain a different number of crypts were increased in diabetic rats. At the end of the experimental treatment, the incidence, number and size of tumors were also increased in diabetic rats. Overall, these data indicated that diabetes increased the risk of colorectal cancer. The activity of HK and PK in colonic tissues was increased in diabetic rats, whereas the activity of PDH was decreased. In addition, the activities of these enzymes in intratumor were higher than that of in peritumor. These data indicated that the high rate of glycolysis may play a role in colorectal carcinogenesis in diabetic rats.
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PMID:Diabetes promotes DMH-induced colorectal cancer by increasing the activity of glycolytic enzymes in rats. 2532 3