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

In Wistar rats just after weaning, 5/6 of renal parenchyma were removed surgically. Thereafter, the rats were fed either a "high-protein" (21%) or two types of a "low-protein" (6%) diet; in one of the latter the lack of protein was substituted by saccharide, in the other by fat, making the substitution "isocaloric" in either case. In all three diet groups, subgroups were formed drinking either tap water or water containing either the ACE inhibitor enalapril (Ena) or the calcium antagonist diltiazem (Dil), or both (Ena + Dil). In the high-protein diet group, increases in the weight of kidney remnants, in proteinuria and in systolic blood pressure (SBP) were seen. This was prevented by feeding either type of the low-protein diet but also by Ena and Ena + Dil. Ena and Ena + Dil not only prevented the increase in SBP but actually lowered it significantly. Dil alone also had a SBP-lowering action but offered no protection from kidney hypertrophy and proteinuria. No additive protective action of Ena + Dil or Ena + low protein or Ena + Dil + low protein was seen, suggesting that a bottom limit of these protective action was reached by the low-protein diet alone. There was no substantial difference between either type of the low-protein diet except a small and transient decrease in body weight in the first week of fat-rich diet administration.
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PMID:A comparison of the effect of feeding a low-protein diet and of pharmacological intervention on the course of ablation nephropathy in the rat. 777 Jun 41

Recent studies have shown that, not only in hypertensive animals but even in normotensive rats, dietary salt (sodium chloride) produces a dose-related increase in the left ventricular and renal mass. In the present study the effects of the angiotensin converting enzyme inhibitor (ACEI) enalapril and the thiazide-type diuretic, hydrochlorothiazide, on the development of the salt-induced left ventricular and kidney hypertrophy were examined in normotensive Wistar-Kyoto and Wistar rats. A high intake of sodium chloride (6% of the dry weight of the chow to mimic the level found in many human food items) during eight weeks produced a marked increase in the mass of the left ventricle and the kidneys in both rat strains with little or no effect on blood pressure. The cardiac hypertrophy correlated strongly with the renal hypertrophy. These salt-induced changes in the heart and in the kidneys were completely blocked by hydrochlorothiazide, while enalapril was devoid of any significant effects during the high-salt diet. However, during a low-salt diet enalapril, but not hydrochlorothiazide, effectively lowered the blood pressure and decreased the left ventricular mass of the normotensive rats. There was a 3- to 4-fold increase in the urinary excretion of calcium during the high intake of sodium chloride. Hydrochlorothiazide decreased the urinary excretion of calcium even during the low salt diet, and it completely blocked the salt-induced hypercalciuria. Enalapril had no significant effect on the urinary calcium excretion. During the low-salt diet hydrochlorothiazide increased the calcium and decreased the potassium concentration in the heart while enalapril increased the phosphorus concentration. In conclusion, a high intake of sodium chloride produced hypertrophy both in the heart and in the kidneys, even in the absence of a rise in blood pressure. Salt also remarkably increased the urinary calcium excretion. These harmful effects of salt were blocked by the thiazide diuretic hydrochlorothiazide but not by the ACEI enalapril. However, this study does not allow to make any direct comparison between the effects of enalapril and hydrochlorothiazide.
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PMID:Effects of enalapril and hydrochlorothiazide on the salt-induced cardiac and renal hypertrophy in normotensive rats. 784 79

In Dahl S rats, high salt intake causes hypertension and cardiovascular hypertrophy and fibrosis, associated with an apparent increase in activity of tissue RAAS. In the current study, we assessed the effects of two AT1-receptor blockers (ARB) on AT1- and AT2-receptors and ACE densities and salt-induced cardiovascular changes. The hydrophilic ARB losartan (30 or 100 mg.kg.d) and the lipophilic ARB telmisartan (10 or 30 mg.kg.d) were administered once daily, and a high-salt diet was provided from 5 to 9 weeks. In Dahl S but not R rats, the high-salt diet caused marked hypertension, cardiac and kidney hypertrophy, and fibrosis. Both ARBs dose-dependently inhibited binding of Ang II to AT1-receptors and reversed the salt-induced increases in AT2-receptor densities in the CNS. Both ARBs at regular doses attenuated the salt-induced hypertension and, at high doses, prevented the increase in BP during the day but not during the night. Both ARBs similarly prevented high-salt-induced interstitial and perivascular fibrosis in the LV and RV as well as fibrosis in the aorta and renal tubules. RV hypertrophy was also prevented, but LV hypertrophy only partially, and kidney hypertrophy not at all. In Dahl S rats, AT1-receptor stimulation seems to play a critical role in salt-induced hypertension and fibrosis, but a lesser role in tissue hypertrophy.
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PMID:Prevention of salt-induced hypertension and fibrosis by AT1-receptor blockers in Dahl S rats. 1841 73