Ignet

Gene Pair Information

Gene Pair: ACE, AGT

Related Sentences

#	PMID	Sentence
1	3325392	Since the angiotensin converting enzyme (ACE) is identical with kininase II, the reduction of its activity by an ACE-inhibitor such as captopril will not only decrease the concentration of angiotensin II but also elevate the levels of kinins.
2	3054274	We review available data on the activity of the renin-angiotensin system (RAS), responsiveness to angiotensin II (ANG II), ANG II receptor number, and effects of inhibition of the RAS by angiotensin I converting enzyme (ACE) inhibitors in patients with diabetes mellitus.
3	2853753	These results indicate that ACE inhibition interferes with the glomerular capillary permeability induced by angiotensin II.
4	2575661	The effect of angiotensin converting enzyme (ACE) inhibition on kidney function in diabetic nephropathy showed that the GFR is not dependent on angiotensin II (Ang II), and that ACE inhibition diminished albuminuria, probably by lowering glomerular hypertension.
5	2693655	Thus, inhibition of Ang II generation may explain why angiotensin converting enzyme (ACE) inhibitors may be effective in arresting or slowing the progression of renal failure in experimental animals and in man.
6	2408249	ACE-inhibitors exhibit their blood pressure-lowering activity not only via a reduction of angiotensin II but also via on increase of kinin levels.
7	2188897	Elevated serum angiotensin converting enzyme activity and plasma renin activity, expressed as generated angiotensin I, were unaffected by the lower dose of insulin, but were reduced by 26% and 40%, respectively at the higher dose.
8	1513111	Whereas plasma renin activity rose in both the perindopril and triple therapy groups, it is likely that the effects on angiotensin II levels were opposite since perindopril but not triple therapy was associated with a significant reduction in plasma angiotensin converting enzyme activity.
9	1457255	This could be explained by the fact that ACE-inhibitors suppress the trophic effects of angiotensin II on the nephron, while calcium channel blockers might interfere with intracellular processes involved in cell hypertrophy that require the interaction of calcium ions.
10	8458051	Patients at greatest risk of declining renal function during therapy with ACE inhibitors are those in whom maintenance of renal function is dependent on angiotensin II.
11	8476260	Angiotensin converting enzyme transforms angiotensin I into angiotensin II and breaks down bradykinin into inactive products.
12	8285177	In particular, ACE inhibitors appear to protect the kidney more than would be expected from simply the lowering of blood pressure and decreasing of intraglomerular pressure, possibly because angiotensin II has both hemodynamic and direct effects on the glomerulus.
13	8285177	Part of these seemingly inconsistent observations may be due to (1) potential activity of tissue RASs, (2) increased sensitivity to angiotensin II in diabetes, or (3) an effect of ACE inhibition on other systems in addition to the RAS.
14	7769497	In particular, ACE inhibitors have actions beyond blockade of angiotensin II formation, necessitating cautious interpretation of data from their use.
15	8800600	Treatment with angiotensin converting enzyme (ACE) inhibitors ameliorates human and experimental diabetic nephropathy, possibly as a result of changes in angiotensin II (AngII) and/or bradykinin concentrations.
16	11115412	Together with the findings that both ACE inhibition and angiotensin II blockade improve resistance vessel function in this group, it is likely that at least some of the beneficial effect is mediated through the angiotensin II/type I receptor pathway.
17	11260405	The high correlation between the renal hemodynamic response to captopril and to candesartan indicates that reduced angiotensin II formation is the main mechanism of action of the ACE inhibitor.
18	11422735	Faster progression to ESRD is associated with the ACE genotype when the total population with ESRD and with the AGT genotype when patients with glomerulonephritis are considered.
19	11508273	Diabetic rats were either untreated or received the angiotensin converting enzyme inhibitor ramipril, or the angiotensin II type 1 receptor antagonist, valsartan.
20	11855793	We compared the efficacy of treatment protocols with an angiotensin converting enzyme (ACE) inhibitor alone (enalapril, 5 mg) or angiotensin II (ATII) receptor blocker (losartan, 50 mg) or both enalapril plus losartan in patients with microalbuminuria in a prospective, randomized clinical trial.
21	11881122	Mean (+/-SD) serum angiotensin-converting enzyme (ACE) activity and plasma angiotensin II(Ang II) levels at days 17-18 of pregnancy were greater in the untreated diabetic rats than in control pregnant rats (ACE: 163+/-18 vs. 111+/-21 nmol/ml/minute, p<0.001, Ang II: 115+/-45 vs. 43+/-10 pg/ml, p<0.005).
22	11881122	Increased serum ACE activity during pregnancy and postpartum in the untreated diabetic rat is associated with enhanced serum Ang II levels, which may contribute to increased protein excretion and renal hypertrophy.
23	11935151	Treatment with ACE-inhibitors attenuates retinal overexpression of VEGF-A in patients with proliferative diabetic retinopathy, probably by interference with a local effect of angiotensin II.
24	12692747	Due to the lack of effective alternative enzyme pathways, blockade of Ang II production may be more effective with renin inhibition than with angiotensin-converting enzyme (ACE) inhibition.
25	12829650	However, the observed deleterious hemodynamic responses to high glucose and Ang II and the insensitivity to ACE inhibition may, taken together, provide an explanation for the adverse renal outcomes in patients with type 1 diabetes and high N/D ratio.
26	15494545	Infusion of ANG II (50 ng x kg(-1) x min(-1)) increased mean arterial pressure by approximately 7 mmHg in all groups of mice and reduced SNGFR in WT and ACE 1/3 mice (to 30.9 +/- 2.8 and 31.9 +/- 2.5 nl x min(-1) x g KW(-1)) while increasing it in ACE 2/2 mice (to 55.3 +/- 5.3 nl x min(-1) x g KW(-1)) despite an increase in total renal vascular resistance.
27	15934924	As increasing the levels of ACE by approximately 50% in this polymorphism is only calculated to increase the levels of angiotensin II by < 5%, whereas the levels of bradykinin will decrease by 20%, bradykinin may be nephroprotective.
28	16503870	In this review the effect of inhibiting the renin-angiotensin system with angiotensin converting enzyme inhibition and a comparison to angiotensin II receptor antagonism is discussed, with the results of clinical trails reflecting the more recently discovered, non-haemodynamic, proatherogenic actions of angiotensin II.
29	16872231	Promising additional strategies include ACE inhibitors and angiotensin II type 1 receptor antagonists because of their effectiveness and good tolerability in patients with migraine, particularly in those with hypertension.
30	16954165	In the analysis of gene-gene interaction, these effects of the AGT 235T homozygotes on HRV sympathetic index were more apparent in the presence of the ACE D allele.
31	17083070	Firstly, angiotensin II (Ang II) and aldosterone produce similar biological effects and Ang II withdrawal has been shown to benefit patients with angina; aldosterone blockade may therefore follow in the footsteps of ACE inhibitors, as it did in heart failure, and produce benefits in vascular patients without heart failure.
32	17307998	Our work suggests that ANG II, formed by the enzymatic activity of ACE and chymase, plays an important role in inducing postischemic LR and LA, effects that involve the engagement of both AT(1) and AT(2) receptors and may be mediated by CGRP and NADPH oxidase.
33	17897017	Angiotensin converting enzyme (ACE) is a key enzyme in the renin angiotensin system (RAS) and converts angiotensin (Ang) I to the vasoconstrictor Ang II, which is thought to be responsible for most of the physiological and pathophysiological effects of the RAS.
34	18326228	To study prevalence and clinical implications of paradoxical rise of angiotensin II (AII) level in blood plasma in long-term therapy with ACE inhibitors in patients with type 2 diabetes mellitus (DM-2) and diabetic nephropathy (DN).
35	18223023	While ACE promotes angiotensin (Ang) II formation from Ang I, ACE2 degrades Ang II and Ang I.
36	18619489	The cardiac action of Ang II is influenced by the activity of different isoforms of ACE leading to different amounts of Ang II by comparison with other angiotensinogen-derived peptides.
37	19034303	Angiotensin converting enzyme (ACE) generates angiotensin II from angiotensin I, which plays a critical role in the pathophysiology of diabetic nephropathy.
38	19124424	There may be a therapeutic rationale to prefer ARBs over ACE-Is in well-selected patients with congestive heart failure (CHF) because a considerable amount of angiotensin II (Ang II) is produced independent of angiotensin-conversion-enzyme (ACE) in the failing heart and is therapeutically unaffected by ACE-I treatment.
39	19107135	However, the blockade of Ang II by perindopril, an angiotensin converting enzyme (ACE) inhibitor, inhibited upregulation of VEGF, and prevented the loss of tight junction proteins.
40	19114589	Inhibitors of the angiotensin-converting enzyme (ACE) decrease angiotensin II production and activate an intracellular signaling cascade that affects gene expression in endothelial cells.
41	19379059	ACE inhibition by perindopril has two main effects: it inhibits the angiotensin II formation and potentiates bradykinin.
42	19929182	In people with screen-detected type 2 diabetes in primary care, (1) to assess adherence to guidelines, recommending consultation with the GP every three months and treatment initiation with an ACE inhibitor or an angiotensin-II receptor antagonist when systolic BP was > 120 mmHg and/or diastolic BP was > 80 mmHg, and (2) to identify predictors for adherence.
43	19942847	Three substance classes that block RAS-activation are currently available, angiotensin converting enzyme (ACE) inhibitors, angiotensin II type 1 receptor blockade (ARB) and renin inhibitors.
44	20479236	The ACE polymorphism does not significantly affect blood pressure or angiotensin II levels, suggesting that the kallikrein-kinin system partly mediates the effects of the polymorphism.
45	20020514	The results suggest that the PJ extract could prevent the development of high blood pressure induced by Ang II in diabetic rats probably by combating the oxidative stress induced by diabetes and Ang II and by inhibiting ACE activity.
46	20799102	Patients in group 1 were exposed to less intensive pharmacological and interventional treatments (aspirin [93.6% vs. 95.3%; p = 0.012], clopidogrel [70% vs. 73%; p = 0.046], unfractionated heparin [59% vs. 65%; p <0.001], ACE inhibitors or angiotensin II antagonists [46% vs. 53%; p <0.001]).
47	12092217	Therapeutic possibilities in renin-angiotensin system control are offered by angiotensin-converting enzyme inhibitors, angiotensin II type-1 receptors antagonists, angiotensin converting enzyme inhibitors and neutral endopeptidase inhibitors and angiotensin II type 2 receptors agonists.
48	19765632	These data show that: (1) HG increases AGT synthesis and activation of renin and ACE by MCTs, leading to local production of Ang I and Ang II. (2) Ang II activates endogenous AT1 and stimulates synthesis of VEGF. (3) HG activation of ERK starts within minutes and lasts for up to 24h.
49	20418269	At variance with angiotensin-converting enzyme (ACE) inhibitors, aliskiren eliminates the main substrate for the 'escape' phenomenon (synthesis of angiotensin II from angiotensin I through alternative enzymatic pathways).
50	14678947	Clinical and animal studies show that treatment with angiotensin-converting enzyme (ACE) inhibitors or ANG II-receptor antagonists slows progression of nephropathy in diabetes, indicating ANG II plays an important role in its development.
51	19846569	Although renal cortical ACE protein activity [2.1 +/- 0.8 vs. 9.2 +/- 2.1 arbitrary fluorescence units (AFU) x mg(-1) x min(-1)] and intensity of immunohistochemical staining were significantly reduced and ACE2 protein activity (16.7 +/- 3.2 vs. 7.2 +/- 2.4 AFU x mg(-1) x min(-1)) and intensity elevated, kidney ANG I (113 +/- 24 vs. 110 +/- 45 fmol/g) and ANG II (1,017 +/- 165 vs. 788 +/- 99 fmol/g) levels were not different between diabetic and control mice.
52	19846569	In control kidneys, afferent arteriole vasoconstriction produced by ANG I was significantly attenuated by ACE inhibition, but not by serine protease inhibition.
53	19846569	In contrast, afferent arteriole vasoconstriction produced by intrarenal conversion of ANG I to ANG II was significantly attenuated by serine protease inhibition, but not by ACE inhibition in diabetic kidneys.
54	20627940	The aim of this study was to evaluate angiotensin-I converting enzyme (ACE) activity and expression in numerous tissues, especially kidney, of non-obese diabetic mouse.
55	21668039	Among different drug classes, angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]) have provided an excellent alternative to ACE inhibitors, representing a more selective and a better tolerated pharmacological approach to interfere with the RAS.
56	21721600	Use of combination pharmacotherapy, including angiotensin-converting enzyme (ACE) inhibitors, angiotensin II type 1 receptor antagonists (angiotensin receptor blockers) and ?-adrenoceptor antagonists (?-blockers) in the management of heart failure (HF) can reduce mortality, prevent functional decline and reduce health service use.
57	21846157	In this review, we provide a brief overview of the renin-angiotensin-aldosterone system (RAAS) and discuss the rationale, clinical evidence, and shortcomings related to the use of angiotensin-converting enzyme (ACE) inhibitors in combination with angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]).
58	21846157	DRIs may be useful in combination with ACE inhibitors or ARBs as they provide a more complete blockade of the RAAS, effectively suppressing residual angiotensin II production and the counter-regulatory increase in plasma renin activity observed in patients receiving monotherapy with ACE inhibitors or ARBs.
59	21950781	Recently, besides the well known therapeutic approaches for RAS blockade, based on the use of ACE inhibitors, angiotensin II type 1 receptor antagonists (angiotensin receptor blockers [ARBs]) and aldosterone antagonists, both the scientific and medical community have focused their attention on a novel therapeutic option.