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

---

Query: EC:3.4.15.1 (ACE)
18,300 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The etiology of afterload elevation in congestive cardiac failure is unclear, but experimental evidence suggests a role for the renin-angiotensin system in maintaining elevated peripheral vascular resistance. The angiotensin converting enzyme inhibitor SQ20,881 was administered to eight patients with congestive cardiac failure (four hypertensives, four normotensives) during or one day after diagnostic cardiac catheterization. Various hemodynamic measurements performed before and during blockade indicate that this agent caused improvement in cardiac function in all patients by decreasing afterload. This improvement correlated with the decrease in total vascular resistance but was independent of the baseline blood pressure and plasma renin activity. These results suggest that inhibition of angiotensin converting enzyme is a worthwhile approach to the treatment of congestive heart failure, although its exact mechanism of action remains unclear.
...
PMID:Angiotensin converting enzyme inhibition in patients with congestive heart failure. 69 46

1. The renal artery of conscious dogs was acutely narrowed over 30 s to reduce renal artery pressure distal to the stenosis to 40 mmHg and the stenosis was maintained for 1 h. The distal renal artery pressure was rapidly restored to a plateau slightly below pre-stenosis values within 10--15 min. Rises in systemic blood pressure and plasma renin activity were small and transient. 2. This restoration was an active process, mediated by the intrarenal effects of angiotensin II (AII), since it was greatly diminished or abolished when the renal artery was narrowed in the presence of angiotensin I-converting enzyme inhibitor or angiotensin receptor antagonist (1-Sar-8-Ile AII). However, it was not diminished by 'total' autonomic effector blockade. 3. This angiotensin II-mediated restoration of renal artery pressure may be of homeostatic significance for the maintenance of glomerular filtration rate.
...
PMID:Intrarenal action of angiotensin II in restoring renal artery pressure after acute renal artery stenosis. 72 9

The aldosterone and arterial pressure response to long-term infusion of two angiotensin II inhibitory analogues, [Sar1,Ala8]angiotensin II and [Sar1,Ile8]angiotensin II, and the angiotensin I-converting enzyme inhibitor, SQ 20,881, was studied in conscious dogs during sodium deficiency. Plasma aldosterone concentration (PAC), plasma cortisol concentration (PCC), and plasma renin activity (PRA) were determined by radioimmunoassay. In conscious dogs after dietary sodium restriction (5 mEq of Na+/day) for 21 days, PAC averaged 37.5 +/- 8.9 (mean +/- SE) ng/dl, PCC averaged 1.3 +/- 0.5 microng/dl, PRA averaged 3.23 +/- 0.42 ng/ml per hour, and arterial blood pressure (AP) averaged 103 +/- 5 mm Hg. During long-term infusion of [Sar1,Ala8]angiotensin II (5 microng/kg min-1), PAC averaged 34.7 +/- 8.5 ng/dl, PCC averaged 1.5 +/- 0.5 microng/dl, PRA averaged 16.4 +/- 3.1 ng/ml per hour, and AP averaged 88 +/- 5 mm Hg. During long-term infusion of [Sar1,Ile8]angiotensin II (5 microng/kg min-1), PAC averaged 45.8 +/- 12.6 ng/dl, PCC averaged 1.75 +/- 0.5 microng/dl, PRA averaged 13.6 +/- 4.3 ng/ml per hour, and AP averaged 86 +/- 5 mm Hg. During long-term infusion of angiotensin I-converting enzyme inhibitor (5 microng/kg min-1), PAC averaged 14.9 +/- 4.8 ng/dl, PCC averaged 1.75 +/- 0.5 microng/dl, PRA averaged 20.3 +/- 5.3 ng/ml per hour, and AP averaged 76 +/- 5 mm Hg. The intrinsic agonistic properties of the angiotensin II inhibitory analogues on the adrenal cortex negate their use for defining the role of the renin-angiotensin system in the regulation of aldosterone biosynthesis during sodium deficiency. The precipitous fall in aldosterone secretion and arterial blood pressure during long-term infusion of angiotensin I-converting enzyme inhibitor demonstrates the importance of the renin-angiotensin system in mediating aldosterone biosynthesis during sodium deficiency and the essential role of the renin-angiotensin-aldosterone system in the regulation of arterial pressure during sodium deficiency.
...
PMID:Role of the renin-angiotensin system in the regulation of aldosterone biosynthesis and arterial pressure during sodium deficiency. 87 Feb 26

1. The blood-bathed organ technique was used to study the release of catecholamines, angiotensin II and prostaglandin-like (PL) substances into the circulation during hypercapnia and after haemorrhage in anaesthetized dogs. 2. Elevated blood concentrations of noradrenaline, angiotensin II and prostaglandin-like substances have been detected during both experimental conditions. 3. The rise of arterial blood pressure during hypercapnia and after haemorrhage was associated with elevated concentrations of angiotensin II in the blood and could be abolished by inhibition of the angiotensin I-converting enzyme with SQ 20881. 4. The compensation of arterial pressure during both stresses was significantly impaired by release of prostaglandin-like substances; it could be restored by inhibition of prostaglandin biosynthesis with indomethacin. 5. The results indicate that activation of the renin-angiotensin system represents the major humoral mechanism for the maintenance of arterial pressure during hypercapnic acidosis and after haemorrhage.
...
PMID:Humoral response and blood pressure regulation during hypercapnia and haemorrhage in dogs. 107 98

The influence of the renin-angiotensin system on the control of cell communication was investigated in isolated ventricular cell pairs of adult rats. It was found that angiotensin II (1 microgram/ml) reduced the junctional conductance (gj) by about 55% within 20 s. This effect of angiotensin II was suppressed by DuP 753--an angiotensin receptor blocking agent. Enalapril (1 microgram/ml)--an angiotensin converting enzyme inhibitor--caused an increase in junctional conductance (106%) within 2 min. The effect of enalapril on gj was not related to activation of beta-adrenergic receptors or cAMP-dependent protein kinase. The effect of angiotensin II on gj was suppressed by staurosporine--a potent inhibitor of protein kinase C. This finding indicates that the peptide is changing gj through activation of protein kinase C. The increase in cell coupling caused by enalapril raises the possibility that the antiarrhythmic action of enalapril as well its effect in congestive heart failure are related to an increase in electrical synchronization of cardiac myocytes.
...
PMID:The role of the renin-angiotensin system in the control of cell communication in the heart: effects of enalapril and angiotensin II. 128 Jul 22

The effects of dopamine on plasma renin-angiotensin-aldosterone system vasopressin levels and blood pressure were studied in anesthetized guinea-pig. The inhibition of the angiotensin converting enzyme with perindopril permitted assessment of the role of the renin-angiotensin system. In perindopril-treated guinea-pigs, the activity of angiotensin-converting enzyme was decreased by 90% with simultaneous increases in plasma renin activity and angiotensin I concentration; aldosterone and vasopressin levels, blood pressure and heart rate were not modified. Dopamine depressed mean arterial pressure by 30% and increased heart rate (8%) in controls. Dopamine infusion did not affect either plasma renin activity or angiotensin I concentration or angiotensin-converting enzyme activity in control animals. But in perindopril pretreated animals it further increased plasma renin activity (88%) and angiotensin I concentration (35%). Finally, in controls, dopamine infusion increased plasma vasopressin concentrations (91%) whereas this increase did not occur in perindopril treated animals.
...
PMID:Endocrine and hemodynamic responses to dopamine infusion in the guinea-pig: effects of ACE inhibition with perindopril. 128 86

Angiotensin-converting enzyme (ACE) inhibitors exert their beneficial effects not only via endocrine mechanisms, but most probably also via interference with autocrine-paracrine actions involving local renin-angiotensin and kallikrein-kinin systems with subsequent autacoid release. Inhibition of ACE (kininase II) results in the reduction of angiotensin II generation and kinin degradation, leading to beneficial cardiovascular effects. Bradykinin and prostacyclin release from isolated rat hearts was increased by local ACE inhibitions with ramiprilat. In different models the bradykinin-mediated effects of ACE inhibition were abolished with the specific B2 kinin-receptor antagonist Hoe 140: The cardioprotective effects of ramiprilat or ramipril such as reduction of postischemic reperfusion injuries in isolated rat hearts or the reduction in infarct size in dogs and rabbits were abolished by coadministration of Hoe 140. Furthermore, left ventricular hypertrophy in rats with aortic banding could be prevented or regression was induced when the ACE inhibitor was given in a non-blood pressure-lowering dose. These beneficial effects were also abolished by Hoe 140. In conclusion, in different experimental models, ACE inhibitors exert cardioprotective effects. An enhancement of endothelial autacoid formation (nitric oxide and prostacyclin) by inhibiting degradation of bradykinin may contribute to these effects.
...
PMID:Role of bradykinin in the cardiac effects of angiotensin-converting enzyme inhibitors. 128 35

ACE-inhibitors improve symptoms and prognosis in patients with heart failure. The V-Heft II trial has demonstrated that the beneficial effect of these agents is superior to unspecific vasodilators. Besides sustained arterial and venous vasodilation the inhibition of the neurohumoral axis is thought to play an important role. Angiotensin II and catecholamines not only exert vasoconstrictor effects, but might also contribute to vascular and myocardial growth. Thus, it may not be surprising that the beneficial effects of ACE inhibitors in heart failure only emerge during long-term therapy rather than after short-term administration. It has been shown that these agents improve blood flow to skeletal muscle during exercise after chronic therapy (not acutely), and there is some preliminary evidence that improvement of endothelial function might be involved in this effect, i.e., by reducing the degradation of bradykinin, an endothelial vasodilator. ACE inhibitors reduce LV hypertrophy, an important risk factor for cardiovascular disease and prognosis. Moreover, there is experimental evidence that ACE inhibitors can prevent and even reverse interstitial fibrosis in the left ventricle. Although the plasma renin activity may be normal in patients with chronic heart failure, recent data using polymerase chain reaction indicate that the tissue cardiac renin angiotensin system is activated in the failing human heart as assessed by measurements of angiotensin converting enzyme mRNA and angiotensinogen mRNA which may be an important target for ACE-inhibition.
...
PMID:[The value of ACE inhibitors in heart failure (mechanism of action)]. 129 Mar 8

We have investigated the effective role of angiotensin II on the renal function and urinary excretion of some prostanoids in healthy women submitted to different conditions of potassium balance. To this aim we have evaluated the effects of an acute inhibition of angiotensin converting enzyme by enalapril (E). The renal function was explored by clearance (cl.) method during induced hypotonic polyuria (oral water load followed by 5% dextrose solution infusion). During 60 min cl. period the urinary PGE2, 6-keto-PGF1 alpha and TxB2 were determined by RIA method. Each subject received paired studies, in absence and presence of E (10 mg administered per os 1 hour before the water load). Basal values of plasma renin activity (PRA) and urinary aldosterone (excreted during the 24 hours before the water load) were also determined by RIA method. This study protocol was applied in normal potassium balance (n = 6) and induced moderate potassium depletion (n = 6). This paper concerns the group in normal potassium balance in both absence (N3) and presence of E (N3.E). All subjects were submitted to normal dietary intake of sodium (150 mmol/d) and potassium (50 mmol/d). The basal values of PRA, urinary aldosterone and plasma electrolytes were in the normal range. The only significant effect produced by E was a reduction in mean arterial pressure, without significant changes in creatinine cl., urinary hydro-electrolyte excretions as well as urinary excretions of prostanoids.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Renal effects of the acute inhibition of angiotensin-converting enzyme. I. 1) Studies during normal sodium and potassium balance]. 129 5

We have investigated the relative roles of angiotensin II on the renal function and urinary excretion of some prostanoids in healthy women submitted to different conditions of potassium balance. To this aim we have evaluated the effects of an acute inhibition of angiotensin converting enzyme by enalapril (E). The renal function was explored by clearance (cl.) method during induced hypotonic polyuria (oral water load followed by 5% dextrose solution infusion). During 60 min cl. period the urinary PGE2, 6-keto-PGF1 alpha and TxB2 were determined by RIA method. Each subject received paired studies, in absence and presence of E (10 mg administered per os 1 hour before the water load). Basal values of plasma renin activity (PRA) and urinary aldosterone (excreted during the 24 hours before the water load) were also determined by RIA method. This study protocol was applied in normal potassium balance (n = 6) and induced moderate potassium depletion (n = 6). This paper concerns the group in potassium depletion in both absence (D4) and presence of E (D4.E). Potassium depletion was induced by adaptation to a normal sodium (150 mmol/d) and low potassium (< or = 10 mmol/d) dietary intake combined to natriuretic treatment. The water and NaCl net losses were restored by 0.9% NaCl solution infusion. The cumulative potassium deficit achieved at the end of the depletive treatment was 214 +/- 54 mmol. This treatment induced significant decrease in basal plasma potassium concentration and increase in PRA without affecting urinary aldosterone and plasma sodium concentration.(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:[Renal effects of the acute inhibition of angiotensin-converting enzyme. I. 2) Studies during moderate potassium depletion]. 129 6


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>

---