Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts: Gene/Protein Disease Symptom Drug Enzyme Compound   Target Concepts: 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)

This paper reviews the evidence for the occurrence of hypertrophy of the renal arterial vessels in experimental and human hypertension. In spontaneously hypertensive rats (SHR), the walls of the interlobar, arcuate and interlobular arteries appear to be hypertrophied in both the "pre-hypertensive phase" and in established hypertension. The lumen diameter of the afferent arteriole in SHR is reduced, but this is probably not due to wall hypertrophy. The renal arterial hypertrophy is not reversed by chronic angiotensin converting enzyme inhibition in SHR, in contrast to findings in other vascular beds. Renal arterial hypertrophy also occurs in other forms of hypertension including in the kidney contralateral to a renal artery stenosis, and in hypertension following sino-aortic denervation. Whilst it is not possible to document changes in wall dimensions of intrarenal arteries during the development of human hypertension, renal haemodynamic abnormalities currently attributed to renal vasoconstriction in early human hypertension are also compatible with renal arterial hypertrophy. These abnormalities include increased resting renal vascular resistance and augmented renal vascular resistance responses to vasoconstrictor agents. It is argued that hypertrophy of renal vasculature to increase pre-glomerular resistance will have dual effects: it will increase total peripheral resistance (the kidneys account for about 20% of total peripheral resistance), and it will effect renal haemodynamics distally in a manner similar to narrowing of the main renal artery. It remains to be shown experimentally whether renal arterial hypertrophy could be the primary cause of some forms of hypertension.
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PMID:Pre-glomerular structural changes in the renal vasculature in hypertension. 758 80

Renovascular hypertension (RVH) remains a leading cause of potentially curable hypertension. Although RVH affects less than 1% of the unselected hypertensive population, between 10% and 35% of appropriately screened patients referred to specialised centres for problematic hypertension may prove to have renovascular disease. Advances in percutaneous transluminal renal angioplasty (PTRA) have renewed interest in developing better noninvasive screening tests for identifying patients with potentially correctable hypertension or renal impairment due to renovascular disease caused by either fibromuscular dysplasia (FMD) or arteriosclerosis. Duplex ultrasound with the two-dimensional Echo-Colour-Doppler technique for measurements of blood flow velocities in the renal interlobar arteries as expressed in the Pulsatility Index (PI) has been evaluated. Experimentally induced changes in renovascular resistance (RVR) in normotensives and in primary hypertensives were registered noninvasively by means of PI-measurements. A significant correlation between the absolute values of PI and RVR was found in hypertensives (r = 0.50, p < 0.002), but not in normotensives. In both groups, the changes of RVR due to angiotensin II infusion and ACE-inhibition were significantly correlated to the changes in PI (normotensives: r = 0.69, p < 0.001, primary hypertensives: r = 0.64, p < 0.001). Normally, the blood flow velocities as expressed by the PI in the renal vasculature of the two kidneys are equal. In hypertensive patients, PI was lower in kidneys with significant renal artery stenosis (RAS) than in kidneys without RAS (p < 0.001). Doppler signals were absent in all kidneys with renal artery occlusion. A bilateral low PI combined with normal side difference in PI may in hypertensive patients indicate bilateral RAS. RVH was correctly diagnosed in 84% of the patients and the presence of RAS in 94%. Provocative testing of an activated renin-angiotensin system by means of an angiotensin converting enzyme inhibitor (ACEI) constitutes the foundation for screening for RVH using gamma camera renography with 99mTc-DTPA as a glomerular filtration marker. In 20 consecutive patients with successfully treated RVH, one-third of the patients were not correctly diagnosed using ACEI-enhanced 99mTc-DTPA gamma camera renography, which indicates that some patients with RVH have compensatory mechanisms to maintain GFR after ACE inhibition. The relationship between the renin-angiotensin system and erythropoietin (EPO) production was studied in 20 patients with RAS and hypertension.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Renovascular hypertension. New diagnostic and therapeutic procedures. 766 14

Unilateral renal artery stenosis can lead to a non-functional kidney which secretes large amounts of renin. Four cases are presented in which the high renin state resulted in hypertension, proteinuria from the intact contralateral kidney, and secondary aldosteronism. The proteinuria was in the nephrotic range, which is unusual in renovascular hypertension, but gradually disappeared after correction of the high renin state by removal of the renin-secreting kidney or administration of an ACE inhibitor. Accordingly, when there is marked proteinuria in the presence of new-onset or rapidly progressive hypertension, hypokalaemic alkalosis, and a high peripheral PRA, renal artery stenosis should be considered since the proteinuria may be reversible after nephrectomy, repair of the ischaemic kidney or medical therapy.
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PMID:Reversible nephrotic syndrome due to high renin state in renovascular hypertension. 773 87

A 43 year old man with inoperable aortic coarctation and severe hypertension requiring near maximal anti-hypertensive treatment was admitted in severe heart failure. After 2 weeks of treatment the heart failure and blood pressure were incompletely controlled and angiotensin converting enzyme (ACE) inhibitor was started. Serum creatinine was normal before starting the ACE inhibitor and on discharge from hospital. The patient was re-admitted a week later with gross fluid retention and in renal failure. In the absence of alternative causes, a diagnosis of ACE inhibitor-induced renal failure was made and treatment was stopped. The patient required haemodialysis for 2 days and within 1 week the renal function had reverted to normal and has remained so for 1 year. We propose that the renal haemodynamics in severe aortic coarctation are similar to those in bilateral severe renal artery stenosis and advise caution in the use of ACE inhibitors for adults with aortic coarctation.
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PMID:Acute renal failure with ACE inhibition in aortic coarctation. 787 Jun 44

We have described a patient, subsequently found to have polyarteritis, whose renin activity was 60 times normal, a level associated with malignant hypertension and severe renal artery stenosis. The severe hypertension and its resistance to multiple medications in the face of a dramatic response to low-dose enalapril imply the renin-angiotensin system was the primary pathophysiologic mechanism. We believe renin activity should be measured in hypertensive patients with polyarteritis. Furthermore, PAN should be in the differential diagnosis of hyperreninemic hypertension. ACE inhibitors should be strongly considered in the management of classical PAN-induced hypertension.
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PMID:Hyperrenin-hyperaldosterone-dependent malignant hypertension in polyarteritis nodosa. 790 25

A considerable number of hormones control renal perfusion to preserve glomerular filtration. We used the "captopril test" to characterize patients with renal-vascular hypertension. This study revealed a group of patients which reacted to 25 mg of captopril with a significant increase of plasma renin activity, but angiography excluded a renal artery stenosis. These patients had significantly more hypertensive organ damage than a control-group, including a significant microalbuminuria. Consequently, we infused a subpressure dose of angiotensin II to investigate its impact on albuminuria in these patients. Although angiotensin II induced hyperfiltration, microalbuminuria was not increased. Because this finding could have therapeutic relevance, we investigated the significance of different antihypertensive drugs (beta-blocker, alpha-blocker, Calcium antagonists, ACE-inhibitor) on microalbuminuria in patients with arterial hypertension. Renal hemodynamics were influenced as expected, but blood-pressure and microalbuminuria were reduced to the same extent by all antihypertensives. In contrast to these results, we could demonstrate significantly different influences of a beta-blocker and an ACE-inhibitor on proteinuria in patients with primary glomerulonephritis. These results suggest different effects of antihypertensive drugs on renal protein excretion depending on the actual disease.
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PMID:[Modification of renal hemodynamics and proteinuria in patients with arterial hypertension and kidney diseases]. 790 76

Isotope renography is a commonly used investigation for the detection of renal artery stenosis (RAS) in hypertensive patients, although its predictive accuracy is poor in an unselected population with a low prevalence of RAS. The aim of the present study was to identify characteristics of hypertensive patients that raise the clinical suspicion of underlying RAS, and which are predictive of an abnormal isotope renogram. The characteristics of 75 patients who had undergone either conventional or ACE-inhibitor-enhanced renography were retrospectively assessed and correlated with the renogram results. The presence of a raised serum creatinine, severe systolic hypertension at presentation and the requirement for triple drug therapy best predicted abnormalities on renography. However, it would appear that the false-positive rate of this investigation is high and its predictive accuracy is poor even in a highly selected group of patients. We conclude that isotope renography is of no practical value in the screening of hypertensive patients for RAS. Renal angiography remains the investigation of choice.
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PMID:Isotope renography in the investigation of renal artery stenosis in hypertensive patients. 791 95

ACE inhibitors have been shown to worsen the kidney damage occurring distal to a renal artery stenosis. To determine if this effect was due to the decrease of arterial pressure or to an inhibition of the formation of angiotensin, we compared the effects of equihypotensive doses of an angiotensin converting enzyme inhibitor (enalapril) and a long-acting calcium antagonist (Ro 40-5967) in 2K-1C rats. The rats were treated for five weeks with either enalapril, Ro 40-5967, or were left untreated. A group of sham operated rats was used as control. At the end of the five-week treatment period, proteinuria, plasma urea and creatinine were measured and quantitative morphometry of the clipped and unclipped kidneys was performed. Ro 40-5967, despite an absence of inhibition of the renin-angiotensin system, worsened the lesions of the clipped kidney to the same extent as enalapril. In contrast, the effects of both drugs on the unclipped kidney were different. Ro 40-5967, and not enalapril, increased the weight and the glomerular surface area of the unclipped kidney. Ro 40-5967 did not change the glomerulosclerosis index, which was improved by enalapril. In contrast with enalapril, Ro 40-5967 decreased plasma urea and creatinine concentrations. Only enalapril decreased proteinuria which originated from the unclipped kidney as shown by nephrectomy experiments. We conclude that during ACE inhibition the fall in renal perfusion pressure seems to be the main determinant of the renal damage distal to a renal artery stenosis, independently of a blockade of the renin-angiotensin system.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Calcium blockade versus ACE inhibition in clipped and unclipped kidneys of 2K-1C rats. 796 54

Angiotensin converting enzyme inhibitor renography (ACE-I-renography) can be used partly to screen for renovascular hypertension and partly to evaluate the possibility for successful revascularization. In patients with an important renal artery stenosis with a high intrarenal activity of the renin-angiotensin-system ACE-inhibition results in a change in renal haemodynamics which can be detected by renography. ACE-I-renography has a high positive and negative predictive value in diagnosing renal artery stenosis. Significant alterations in the renogram induced by ACE-inhibition in renal artery stenosis seem to have a good predictive value with regard to the effect of correction of the stenosis. ACE-I-renography is recommended in patients with arterial hypertension and a moderate or high probability for renovascular hypertension based on clinical criteria.
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PMID:[Angiotensin-converting enzyme inhibitor renography. Physiopathological, diagnostic and therapeutic aspects in renal artery stenosis]. 800 37

The predominant trend in pediatric antihypertensive management is towards increasing reliance on angiotensin converting enzyme (ACE) inhibitors and calcium channel blockers because of their general effectiveness, low incidence of adverse reactions and potential specific benefit in patients with renal disease. The common aetiological relationship between renal disease and elevated BP also is the reason that diuretic therapy continues to be included in many treatment regimens. A number of ACE inhibitors are available for clinical use, although only captopril has been subjected to any meaningful degree of investigation in children. Initial doses of captopril are 0.5 mg/kg in children > 6 months of age and 0.01-0.1 mg/kg in neonates, because of an apparent increased antihypertensive effect and duration of action in this age group. Side-effects are few and the major adverse effect is a reduction in glomerular filtration in patients with bilateral renal artery stenosis. The calcium channel blockers reduce cytosolic calcium concentration and are particularly effective in patients with volume dependent forms of hypertension. The pharmacokinetic properties of these drugs are similar with drug clearance by hepatic metabolism. In particular, nifedipine has a rapid onset of action and is widely used to treat hypertensive emergencies. Although it has been used sublingually, the effectiveness of the drug is due to absorption from the gastrointestinal tract. Few side-effects from these drugs have been reported in children. Heart rate and cardiac output increase but return to pretreatment levels within a few weeks. As is the case with the ACE inhibitors, calcium channel blockers appear to have a positive effect on renal function.
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PMID:Clinical pharmacology of converting enzyme inhibitors, calcium channel blockers and diuretics. 806 88


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