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)

There is increasing evidence that activation of the plasma contact system that results in the production of bradykinin plays an important role in contrast material systemic reactions. The effects of bradykinin in anaphylaxis depend on its rate of destruction and its rate of production. The highest percentage of contrast material reactions occur after intravenous injections, and the major enzyme hydrolyzing bradykinin (kininase II; angiotensin-converting enzyme) is found on pulmonary vascular endothelial surfaces. The inhibitory effects of numerous ionic and nonionic contrast material solutions on the enzyme have been determined. Additionally, the role in this inhibition of the chelators found in all commercial contrast material vials has been studied. In vitro, all such preparations combined with their chelators inhibit angiotensin-converting enzyme. Whether this inhibition plays a role in vivo remains to be established.
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PMID:Inhibition of angiotensin-converting enzyme by contrast media. I. In vitro findings. 235 33

Bradykinin (BK) is widely believed to play a role in the pathogenesis of anaphylaxis. To help clarify any such roles, we examined for effects of inhibitors of kininase II (angiotensin converting enzyme, ACE) and "kininase I" (carboxypeptidase N, CPN), on the early course of egg albumin-induced aggregate anaphylaxis in anesthetized guinea pigs. In this model, pulmonary and systemic arterial blood pressure (BP) rise (unless pulmonary fibrillation occurs), lung wgt increases by approximately 60% and pulmonary microvessels are occluded by cell-rich thrombi, all within 5 min of i.v. antigen. The 30 min mortality rate is approximately 2%. ACE inhibitors (BPP9a, Captopril and MK 422; doses up to 140 mumol/kg) do not make anaphylaxis more nor less severe in terms discernible by changes in BP, lung wgt, EKG or intravascular coagulation. In marked contrast, an inhibitor of CPN (2-mercaptomethyl-3-guanidinoethylthiopropionic acid, 2-MGP; 8-16 mumol/kg) increases the 30 min mortality rate to 94% and lung wgt to 180% of control. The animals die in ventricular fibrillation. Given the enormous BK potentiating effects of BPP9a, Captopril and MK 422, it seems likely that little if any BK is formed in the early min of anaphylaxis. 2-MGP does not potentiate BP effects of BK but markedly potentiates effects of C3a anaphylatoxin. Thus, our data support the views that BK is neither a primary nor secondary mediator of aggregate anaphylaxis, and the adverse effects of 2-MGP are best explained in terms of preservation of anaphylatoxins and not in terms of preservation of kinins.
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PMID:Aggregate anaphylaxis and carboxypeptidase N. 302 62

Cardiac anaphylaxis, an acute ischemic dysfunction comprising coronary vasoconstriction and arrhythmias, is a model of clinically recognized immediate hypersensitivity reactions affecting the heart. Bradykinin, a mediator of hypersensitivity, is also a potent coronary vasodilator, acting via nitric oxide and prostacyclin production. Because ischemia increases bradykinin outflow from the heart, we questioned whether bradykinin might mitigate anaphylactic coronary vasoconstriction. Antigen challenge of hearts isolated from presensitized guinea pigs was associated with an approximately 30% increase in bradykinin overflow. Furthermore, (1) when the half-life of bradykinin was prolonged with the kininase II/angiotensin-converting enzyme inhibitors captopril and enalaprilat, anaphylactic coronary vasoconstriction was attenuated and reversed, and arrhythmias were alleviated; (2) the bradykinin B2-receptor antagonist HOE 140 prevented these effects; and (3) HOE 140 exacerbated both anaphylactic coronary vasoconstriction and arrhythmias. During cardiac anaphylaxis, the coronary overflow of cGMP, a marker of nitric oxide production, and 6-ketoprostaglandin F1 alpha, a stable prostacyclin metabolite, increased two-fold and fourfold, respectively. Because neither enalaprilat nor HOE 140 affected these changes, the enhanced overflow of cGMP and 6-ketoprostaglandin F1 alpha is likely to reflect the actions of other hypersensitivity mediators (eg, histamine and leukotrienes). We postulate that bradykinin plays a protective role in cardiac anaphylaxis by accumulating at the luminal surface of the coronary endothelium and promoting, in an autocrine mode, a B2-receptor-mediated production of nitric oxide and prostacyclin in concentrations sufficient to elicit a paracrine effect on coronary vascular smooth muscle, thus opposing the vasoconstricting effects of other anaphylactic mediators.
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PMID:Protective role of bradykinin in cardiac anaphylaxis. Coronary-vasodilating and antiarrhythmic activities mediated by autocrine/paracrine mechanisms. 785 89

Markers of immediate-type hypersensitivity such as histamine and tryptase were measured in the plasma of nonallergic volunteers and patients with a history of hymenoptera venom anaphylaxis. No significant differences in histamine or tryptase were found between patients and controls. Norepinephrine, an important compound involved in the control of cardiovascular functions and blood pressure, was the same in patients and nonallergic volunteers. In addition, components of the renin-angiotensin system were determined. Patients with hymenoptera venom anaphylaxis showed significantly lower plasma angiotensinogen concentrations as compared to healthy nonallergic controls (p < 0.007), whereas plasma ACE activity was the same. Likewise, the plasma levels of angiotensin I and angiotensin II were significantly reduced in patients as compared to controls (p < 0.04 and p < 0.003, respectively). These findings suggest that the renin-angiotensin system may play an important role as a counteracting factor in hymenoptera venom anaphylaxis.
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PMID:Histamine, tryptase, norepinephrine, angiotensinogen, angiotensin-converting enzyme, angiotensin I and II in plasma of patients with hymenoptera venom anaphylaxis. 791 43

Taken together, with the wide-spread use of ACE-inhibitors within the dialysis population, a novel type of hypersensitivity reaction has been recognized, which may occur not only during hemodialysis but also during other forms of extracorporeal therapy. From the data available today, it seems that such reactions are triggered by negatively charged biomaterials which are capable to activate factor XII, leading among others to the generation of bradykinin. Normally this kinin is rapidly degraded by the serine proteinase kininase II. Thus, in the absence of ACE inhibitors plasma bradykinin levels increase only moderately during dialysis with AN69 membranes and clinically most patients are free of symptoms. However, once kininase II, which is identical with converting enzyme, is blocked by ACE inhibitors, plasma levels may increase more than 100-fold and patients will suffer from severe anaphylaxis. Based on our present knowledge, the consequences for clinical medicine are straightforward. It is mandatory to avoid the combination of negatively charged membranes or other biomaterials with ACE inhibitor therapy. As there are many different membranes available, this should be no unsurmountable problem in the setting of clinical hemodialysis.
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PMID:Anaphylactoid reactions during hemodialysis. 792 83

We report a case of a 58-year-old woman who had angiotensin converting enzyme inhibitor-induced angioedema after she underwent a biopsy of a hypopharyngeal mass. The angioedema was associated with severe transient myocardial dysfunction documented on echocardiography. She did not have anaphylaxis or coronary artery disease. To our knowledge this is the first reported case of transient myocardial dysfunction in the setting of angiotensin converting enzyme inhibitor-induced angioedema without anaphylaxis.
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PMID:Transient myocardial dysfunction associated with angiotensin-converting enzyme inhibitor-induced angioedema: recognition by serial echocardiographic studies. 1058 89

It has been discussed in several studies that non-immunologic factors, such as renin angiotensin aldosterone system (RAAS) may play a role in the pathophysiology of anaphylaxis. This study aimed to determine whether RAAS plays a part in the fall in blood pressure during drug reactions or not. Twenty patients who experienced hypotension during drug reaction and 15 healthy volunteers were enrolled in this study. None of the patients in the study or control groups were under treatment with any drug that was capable of influencing to RAAS. Serum levels of angiotensin-I (A-I), angiotensin-II (A-II), angiotensin converting enzyme (ACE) and aldosterone were measured in both study and control groups. The Mann-Whitney U test was used to compare the results of the groups. There were no statistically significant differences between the groups with respect to A-I, A-II, ACE and aldosterone levels. It was concluded that a fall in blood pressure during drug reaction must be the result of mast cell mediator effects on the vascular wall rather than RAAS impairment.
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PMID:Renin angiotensin aldosterone system and drug allergies complicated with hypotension. 1092 19

This case presented the scenario of a patient who had severe bronchospasm from an unknown etiology. Further, she had difficulty speaking and denied any past medical history, which made a diagnosis more difficult. Prehospital providers were challenged with determining the differential diagnosis for bronchospasm and hypoxemia. Was the patient experiencing an anaphylactic reaction, acute asthmatic attack or something else? The key here, once again, is conducting a thorough assessment and patient history. Remember, all that wheezes is not asthma; therefore, providers in this case had to determine if the patient was suffering something such as anaphylaxis, asthma, bronchitis, pneumonia or even congestive heart failure (CHF). Typically, anaphylaxis and asthma affect ventilation, not oxygenation, so until the late stages of anaphylaxis or asthma, the patient will have difficulty moving air, but will be oxygenating OK. We understand that many respiratory conditions can cause wheezing, but CHF? Yes: As left ventricular function diminishes and leads to increased pulmonary pressure, serum begins to leak out of the pulmonary vessels and into the interstitial space. As the interstitial pressure increases, it causes narrowing of the bronchioles, and air traveling through the narrowed bronchioles causes the wheezing sound. Fluid may also be leaking out of the pulmonary capillaries and occupying space in the alveolar sacs. When the interstitial pressure is high and the bronchioles continue to narrow, providers may initially hear only the wheezing and not the crackles from the smaller airways. In these conditions, oxygen is not exchanged adequately into the blood, and the patient becomes hypoxemic. Good assessment and patient history will guide the EMS provider to the cause of bronchospasm. For example, does the patient have a history of asthma? If yes, asthma is likely to be the cause. Does the patient have any rash, hives or swelling? If yes, anaphylaxis is likely the cause. Is the patient elderly, and does he/she show pedal edema, JVD, hypoxemia and/or distended neck veins? If yes, CHF may be the cause. [table: see text] There are questions regarding the use of bronchodilators in patients suffering CHF. If a CHF patient is wheezing (bronchospasm), then a beta-2 selective breathing treatment may be appropriate, along with nitrates and diuretics. Oxygenation is the critical problem in CHF, and hypoxemia will continue to worsen cardiac function. Remember, both bronchoconstriction and alveolar sacs filling with fluid will impair oxygenation of the RBCs and ultimately the vital organs. Focused prehospital management of CHF is aggressive in restoring oxygenation. For example, many agencies are now using oxygen, nitrates, ACE inhibitors and CPAP. By better understanding the pathophysiology of respiratory emergencies and their differential diagnosis, we will improve patient outcomes.
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PMID:Breathless. 1196 14

Anaphylactic and anaphylactoid reactions related to haemodialysis have been increasingly described for almost 3 decades. The majority of these cases used to occur with ethylene oxide sterilized, and complement-activating cellulose membranes. However, a considerable number of publications have focused on polyacrylonitrile AN69 high flux membranes, angiotensin converting enzyme inhibitors and iron as other important causes of potentially severe haemodialysis-related anaphylactoid reactions. Clinical manifestations vary considerably and generally do not allow differentiation between IgE-mediated anaphylaxis and anaphylactoid reactions (e.g. from nonspecific mediator release). Successful management of these patients requires multidisciplinary approach and involves prompt recognition and treatment by the attending physician, and identification of the offending agent(s) with subsequent avoidance of the incriminated compound(s). This review focuses on some major causes of anaphylactoid and anaphylactic reactions during haemodialysis. Special consideration is given to the therapeutic and diagnostic approach.
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PMID:Haemodialysis-associated anaphylactic and anaphylactoid reactions. 1640 99

Angioedema can be a symptom of anaphylaxis; it may be more hazardous that the circulatory collapse in otherwise healthy patients. Angioedema can be part of IgE- and histamine-mediated allergic reactions or part of NSAID-induced hypersensitivity with disturbances in arachidonic acid metabolism. If angioedema occurs without urticaria or other symptoms of anaphylaxis, it is usually mediated by increased bradykinin synthesis (HANE, EANE) or reduced metabolism (ACE inhibitors). These observations have led to new therapeutic approaches in HANE. Icatibant is a bradykinin-receptor-2 antagonist and blocks bradykinin-induced angioedema in HANE. How applicable this will be to ACE-inhibitor angioedema remains to be seen.
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PMID:[Angioedema]. 1800 29


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