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)

The influence of a new ACEI, Ramipril (R) on renal handling of UA was investigated. 13 hypertensives with normal renal function received either R (10 mg p.o.) or placebo (P). Arterial pressure (AP), GFR (Inulin clearance), Renal Plasma Flow (RPF, PAH clearance), UA urinary excretion (UAV) and fractional clearance (FeAU: UA clearance/GFR) were studied for seven hours after drug administration. GFR remained stable in all cases. R had no effect on sodium excretion rate. Compared to P, R significantly increased UAV by 25 p. 100, FeAU by 32 p. 100, RPF by 26.5 p. 100 and decreased mean arterial pressure (MAP) by 10 p. 100. ACE activity was maximally suppressed at 2 hours. More than 80 p. 100 of the maximal changes in UAU and FeAU were observed within the first two hours, while a progressive increase in RPF up to the fifth hour, and a progressive fall in MAP up to the fourth hour was evident. Except for PAM, all these changes were still present at the end of the study (seventh hour). In conclusion, Ramipril increases the fractional excretion of uric acid. This effect is observed independently of any change in sodium balance and preceeds by two to three hours the changes in renal hemodynamics. The simultaneous changes in FeAU and in ACE activity indicate that the effect on uric acid excretion is presumably due to the fall in angiotensin concentration.
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Influence of acute administration of ramipril on the excretion of uric acid]. 295 32

The effects of three doses of perindopril (4.8 and 16 mg), a new angiotensin I-converting enzyme inhibitor, and of a placebo on systemic blood pressure, heart rate, brachial artery flow and diameter, forearm vascular resistance and the renin angiotensin system biological parameters (plasma converting enzyme activity PCEA, renin activity PRA and aldosterone PA) were compared during a double-blind cross-over study performed in six healthy volunteers. Perindopril dose-dependently inhibited PCEA, increased PRA, augmented brachial artery flow and diameter and decreased forearm vascular resistance, whereas it did not affect systemic blood pressure and heart rate. The perindopril-induced increase in brachial artery flow was related (a) at the low dose to the sole arteriolar and (b) at the two highest doses to both arteriolar and large vessels dilatation. Finally, during the ten first hours following drug intake, there was a significant correlation between perindopril-induced PCEA inhibition and brachial artery flow increase.
Arch Mal Coeur Vaiss 1986 Jun
PMID:[Peripheral hemodynamic and biological effects of perindopril in the healthy subject. Dose-effect relationship]. 302 73

The use of angiotensin converting enzyme inhibitors may lead to reversible renal insufficiency in transplant patients with transplant renal artery stenosis (TRAS). We assessed acute effects of captopril (50 mg, p. os) in 7 cadaver kidney recipients (mean age: 35.6 +/- 4 yrs) with TRAS, 9 to 46 mo after transplantation. All patients were treated by prednisolone and azathioprine. After captopril administration, mean arterial pressure decreased from 127 +/- 6 to 119 +/- 7 mmHg, effective renal plasma flow from 152 +/- 19 to 118 +/- 19 ml/min/1.73 m2, glomerular filtration rate from 59 +/- 8 to 39 +/- 10 ml/min/1.73 m2 and filtration fraction from 0.39 +/- 0.02 to 0.32 +/- 0.07. Among the 7 patients, 2 developed immediate and transient anuria; 4 presented a net decrease of GFR, only one had stable GFR. This patient was chronically treated by captopril; as BP was not controlled, furosemide (40 mg p. os) was added. Serum creatinine increased from 180 to 250 mumol/l. Percutaneous angioplasty was done without decrease in BP; however, treatment by captopril and furosemide could be reinstitued without deterioration in renal function. We conclude that: acute renal failure in kidney graft recipients with TRAS is frequent, but not mandatory; sodium depletion induced by diuretics enhances the fall in GFR; acute effect of captopril must be assessed in patients with TRAS before the use of this product as long term antihypertensive treatment.
Arch Mal Coeur Vaiss 1986 Jun
PMID:[Hypertension and stenosis of the graft artery: effects of conversion enzyme inhibition]. 309 7

The purpose of study was to investigate the role of angiotensin II in idiopathic primary aldosteronism (IPA) and to evaluate the interest of angiotensin converting enzyme inhibitors (ACEI) in its management. The study concerned 10 hypertensive patients, mean 49 +/- 11 years with idiopathic primary aldosteronism due to bilateral adrenal hyperplasia: plasma renin activity (PRA) less than 1.5 ng/ml/h and plasma aldosterone (PA) greater than 25 ng/100 ml. Adrenal venography and adrenal vein aldosterone levels demonstrated bilateral hyperplasia. PRA and PA were evaluated in recumbent position, then after 4 hours in upright posture. The next day, a "captopril screening test" was performed with PA assays before and three hours after a single oral administration of captopril (1 mg/kg). Upright PRA and PA were slightly increased and acute administration of captopril reduced significantly PA levels in all patients. Blood pressure (BP was unmodified under captopril. These hormonal results demonstrated that adrenal glomerulosa remained sensitive to low concentrations of angiotensin II, and underlined the potential interest of ACEI in the management of IPA. Brown R. demonstrated already an increase of adrenal sensitivity to angiotensin II infusions, and isolated an aldosterone-stimulating factor (ASF). Plasma aldosterone levels were related to increased ASF concentrations but there was no link between PRA and ASF. Carey R. suggested that ASF acts through an increase of the sensitivity of aldosterone production to angiotensin II.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1987 Jun
PMID:[Influence of angiotensin on the secretion of aldosterone in idiopathic hyperaldosteronism]. 311

At present we do not possess a specific marker of broncho-pulmonary cancers. We propose to test the specificity of six serum markers labelled by radio-immunological methods (CA-50, CA-19.9, CA-125, CA-15.3, enolase, ACE) in 60 patients suffering from non-tumoural broncho-pulmonary disorders: chronic airflow obstruction = 28, acute infective bronchopulmonary disorders = 23, allergy = 9. We have not found any correlation between the percentage of false positives and sex, age or smoking. On the other hand, the CA-125 was often found to be positive in cases of acute pneumonia. Overall the frequency of false positives with ACE (3.3%) enolase (6.7%) and CA-15.3 (5%) is weak. The threshold of positivity obtained is adequate. This is not the case with CA-50 (33.3%), CA-19.9 (13.3%) and above all CA-125 (53.3%), for these we suggest new thresholds of positivity.
Rev Mal Respir 1988
PMID:[Blood levels of CA-50, CA-19.9, CA-125, enolase, CA-15.3 and carcinoembryonic antigen in non-cancerous bronchopulmonary pathology]. 321 89

Cough is a well recognised though undesirable side effect during the course of treatment with angiotensin converting enzyme inhibitors (IEC). With the help of two examples we have tried to show that this cough does not have an immunological origin but rather pharmacological. Cough was suppressed by non steroidal anti-inflammatory drugs. Stemming from these observations and from two studies in the literature a patho-physiological mechanism for the cough is proposed in which treatment with IEC leads to a connection with prostaglandins, notably bronchial PGE2.
Rev Mal Respir 1988
PMID:[Cough provoked by angiotensin-converting enzyme inhibitors. Effect of non-steroidal anti-inflammatory agents]. 321 98

The isolated perfused rat kidney (IPRK) releases kallikrein in urine and renin in perfusate. We have previously shown (Kidney Int 24: 58-65, 1983) and confirm here that kallikrein, as well as renin releases are influenced by changes in renal hemodynamics in this model: a rise in perfusion pressure (PP) from 80 to 98 mmHg increases renal perfusate flow (RPF) by 48 +/- 3 p. 100, inhibits renin release and stimulates kallikrein secretion to 234 +/- 84 p. 100 of control values (n = 8). Since the perfusate lacks angiotensinogen, we decided to study the effect on kallikrein of the reconstitution of the renin-angiotensin system in the IPRK by adding angiotensinogen + angiotensin converting enzyme (AG + ACE) to the perfusion medium. After AG + ACE, PP rose to 107 +/- 4 mmHg, RPF decreased by 82 +/- 3 p. 100 as a consequence of the vasoconstrictor effect of angiotensin II, and renin release was suppressed. Again kallikrein secretion was stimulated and increased to 333 +/- 153 p. 100 of control values (n = 4). It is concluded 1) that kallikrein release is influenced by changes in PP but not in RPF on the IPRK. 2) that reconstitution of the renin-angiotensin system by addition of AG + ACE to the perfusate leads to vasoconstriction, suppression of renin release and a marked increase in kallikrein secretion.
Arch Mal Coeur Vaiss 1985 Oct
PMID:[Kallikrein secretion by the isolated perfused rat kidney. Role of perfusion pressure and the renin-angiotensin system]. 393 40

In the rat model of hypertension induced by a clip on the right renal artery, sparing the left kidney, we compared the efficacity and the endocrine, renal and cardiac effects of classical therapy (CT) of hypertension (Clonidine 0.2 mg/kg and Dihydralazine 15 mg/kg in 2 daily subcutaneous injections and Furosemide 30 mg/kg/day in the drinking water), with inhibition of the angiotensin converting enzyme with a new drug, the S-9490-3 (0.5 mg/kg in one daily administration). The untreated animals (HT: n = 12) had an average systolic blood pressure (SBP) of 215 +/- 32 mmHg. After 1 month' treatment, S-9490-3 (n = 13) lowers SBP to 144 +/- 32 mmHg compared to CT (n = 12) which lowered SBP to only 172 +/- 18 mmHg. The average plasma renin concentrations of the HT animals was four times the normal value (39 +/- 33 ng/ml/h) and both treatment regimes increased it further (S-9490-3: 129 +/- 65 ng/ml/h; CT: 97 +/- 73 ng/ml/h). Angiotensin levels fell in proportion to the increase in renin concentration. Plasma aldosterone was normalised by S-9490-3 (460 +/- 320 pg/ml) but remained as high after CT (850 +/- 650 pg/ml) as in the untreated HT animals (830 +/- 260 pg/ml). Despite the Furosemide, plasma volume increased significantly in the CT group.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1984 Oct
PMID:[Comparison of the cardiac, renal and endocrine effects of converting enzyme inhibition with those of a classical triple therapy in experimental renal hypertension]. 609 34

The natural history of sarcoidosis is favourable in 90% of cases; in 10% deterioration occurs with the appearance of respiratory failure, aspergillous or tuberculous infections which cause death in 5% of patients. Thus the problem for the clinician is the early detection and treatment of those patients whose outcome will be unfavourable. Certain clinical pointers exist measuring the activity and the dissemination of the sarcoidosis as well as its consequences. Among these are radiology, biological tests (such as the serum angiotensin converting enzyme of differential cell counts on bronchoalveolar lavage), scintigraphy and respiratory function; despite the above it is more difficult to determine the prognosis early as in practice this is decided by repetitive screening tests. Steroid therapy seems more effective than other treatments. But drugs cannot be held responsible for those cures which occur apparently unrelated to the treatment received; the occurrence of relapses after interruptions of treatment demand prolonged treatment if an unfavourable outcome is suspected.
Rev Fr Mal Respir 1983
PMID:[Why, when and how to treat sarcoidosis?]. 630 28

Trends in basic research in thoracic medicine are increasingly orientated to biochemical and cellular studies. The need for "biochemical markers" as evidence of a particular type of cell is soon appreciated, both from a qualitative as well as quantitative viewpoint. The ideal criteria which these "markers" should possess (specificity for the organ and cell population and reflecting a well defined metabolic activity) are unfortunately rarely satisfied; the "marker" may be analysed in plasma or broncho-alveolar lavage liquid. Two examples are presented and the difficulties of their interpretation are discussed. First in relation to the determination of serum angiotensin converting enzyme activity and then elastolytic activity in the broncho-alveolar liquid. A good knowledge of basic biological phenomena is necessary to take full advantage of the information which can be obtained by measuring "markers" of activity or function of pulmonary cells.
Rev Fr Mal Respir 1983
PMID:[Markers of cell populations in the lower lung]. 630 29


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