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 investigation is devoted to explore the 24-h patterns of serum angiotensin converting enzyme (ACE) activity in clinically healthy subjects and migraine patients taking as reference the adrenal cycle. Time data series have been analyzed by means of chronobiologic procedures. The biostatistical approach has documented that the enzymatic activity of serum ACE in clinically healthy subjects changes with a circadian periodicity. The chronobiologic approach has additionally revealed that the enzymatic activity of serum ACE activity is circadianly aperiodic in migraine patients, while plasma cortisol shows a preserved cyclicity along 24-h scale. The aperiodicity suggests that the enzymatic degradation of the ACE-dependent substrate is inappropriate over the 24-h span.
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PMID:Chronopathology for angiotensin converting enzyme circadian rhythm in migraine. 216 25

Angiotensin I and II inhibited the nerve stimulation-induced pressure changes in isolated, perfused rabbit ear artery with an IC50 of 3.07 and 0.36 nM, respectively. Neither angiotensin I nor angiotensin II affected the basal pressure or the pressure changes elicited by exogenously administered norepinephrine (NE). The potency of angiotensin I was unaltered by 10(-5) M captopril, indicating that conversion by angiotensin converting enzyme (ACE) was not necessary and did not take place. [Sar1,Val5,Ala8]angiotensin II (3 x 10(-8) M) antagonized the effect of angiotensin I. These findings could have implications regarding ACE inhibitor therapy and the pathophysiology of migraine.
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PMID:Inhibition of neurotransmission by angiotensin I and II in rabbit isolated ear artery. 216 54

We have presented the case of a 37-year-old white man who had recurrent, unilateral, facial edema, temporary partial facial nerve palsy, sensory loss along the ophthalmic and maxillary divisions of the fifth cranial nerve, ageusia bilaterally on the anterior two thirds of the tongue, right extraocular muscle palsies, and intractable migraine-type headaches, leading to the diagnosis of Melkersson-Rosenthal syndrome. The serum angiotensin converting enzyme levels, which are postulated to derive from undiscovered granulomas, were found to be elevated. Methotrexate therapy mitigated the clinical course of the disease, and may prove to be useful in the treatment of this rare and recalcitrant condition.
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PMID:Melkersson-Rosenthal syndrome: elevations in serum angiotensin converting enzyme and results of treatment with methotrexate. 253 97

In 1988 the fourth Joint National Committee (JNC IV) issued new guidelines for the detection, evaluation, and treatment of hypertension. Pharmacologic along with nonpharmacologic therapy is indicated for hypertensive patients whose diastolic blood pressures average greater than or equal to 95 mmHg over a period of time and for patients who have a diastolic blood pressure of 90 mmHg to 94 mmHg with evidence of target organ disease and/or other major risk factors. In the absence of target organ disease and/or other major risk factors, a trial of nonpharmacologic treatment is recommended for patients with a diastolic blood pressure of 90 mmHg to 94 mmHg. The JNC IV report recommends initiating pharmacologic treatment with any one of the following classes of drugs: diuretics, beta blockers, calcium channel blockers, or ACE inhibitors. In general, diuretics and calcium channel blockers are especially indicated for elderly and black patients and beta blockers and ACE inhibitors for young and white patients, but there are many exceptions. In selecting the appropriate step-one agent for a given patient, the therapeutic "two-for-one" concept is emphasized whereby one antihypertensive drug may also be beneficial for a coexisting condition. Examples are: diuretics or ACE inhibitors in congestive heart failure; calcium channel blocking drugs or beta blockers in angina pectoris or paroxysmal supraventricular tachycardia; and beta blockers for migraine headache or senile tremor.
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PMID:Mild hypertension: critical analysis of different therapeutic approaches. 266 23

Normotensive and hypertensive headache sufferers were treated with D-phenylalanine, aprotinin or captopril--all inhibitors of endogenous opioid degradation. Inconsistent results were obtained using D-phenylalanine and aprotinin (acute administration at the start of a migraine attack). Satisfactory results were obtained by prophylactic treatment with captopril (an inhibitor of the angiotensin converting enzyme and of the dipeptidyl carboxypeptidase--an enkephalin inactivating enzyme) compared with conventional drugs such as methysergide, lisuride, pizotifen, clonidine and beta-blocking agents. Excellent results were obtained with captopril on patients suffering from headache and arterial hypertension who had experienced no relief from beta-blocking agents and clonidine. Captopril could thus be a drug of choice in the therapy of headache associated with essential hypertension.
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PMID:Enkephalinase inhibition relieves pain syndromes of central dysnociception (migraine and related headache). 618 94

Presentation of drugs most worthy of interest in autumn 1995. Among these, the ACE inhibitors, the HMGCOA inhibitors, the Proton Pump inhibitors, the serotoninergics used against depression and migraine, the endobronchial corticoids and finally the ASA. Review of their successes, failures and uncertainties.
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PMID:[Leading drugs in 1995: success, failures and uncertainties]. 748 Dec 49

Seventeen patients with migraine headaches, occurring at least twice a month, were successfully treated with an ACE inhibitor for prophylaxis. Most were given enalapril, some used lisinopril. Duration of treatment ranged from 3 months to 3 years. Side effects were generally not noted. Cough occurred in four patients. The mechanism of action is unknown. The lack of side effects and the presence of clearly sustained benefit in this small group of migraineurs should prompt further study and use of this class of drugs for prophylaxis.
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PMID:ACE inhibitors for prophylaxis of migraine headaches. 759 40

A 48-year-old male patient, a surgeon, displayed a right temporo-occipital cerebral haematoma (5 x 7 cm). He had a history of chronic left occipital migraine-like cephalalgia from the age of 16 and hypertension was diagnosed when he was 42 years old. As therapy, he used ACE inhibitors, nifedipine and clonidine for hypertension and for cephalalgia a combination of aspirin, phenacetin and caffeine. During the last 2-3 months before the detection of cerebral haematoma, injections with piritramide were made when severe headaches were unbearable. The patient was operated on the 7th day since the onset of cerebral haematoma after a "wait and see" period of repeated clinical and CT-scan assessment. The initial option of the patient was surgical. We consider that the patient's profession (medical/surgical profile) may have played a positive motivation for the surgical option.
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PMID:Option for surgical management of cerebral haematoma: case report. 777 46

The prevention and treatment of hypertension remain as major challenges for clinicians all over the world. The recently published Sixth Report of the Joint National Committee for the Prevention, Detection, Evaluation and Treatment of High Blood Pressure (JNC-VI) uses evidence-based medicine in providing guidelines to aid clinicians in the prevention, detection and treatment of high blood pressure, including pharmacological approaches. Calcium antagonists are used widely for the treatment of hypertension, and JNC-VI focuses on specific situations where calcium antagonists could be considered as preferred treatments. There are a large number of calcium antagonists available, with a variety of pharmacodynamic and pharmacokinetic actions. Several sustained-release formulations of these drugs are also available. In terms of blood pressure control, calcium antagonists are more effective as antihypertensive treatments than beta-blockers, ACE inhibitors and angiotensin II receptor blockers in Black patients. The dihydropyridine calcium antagonists have been shown to reduce morbidity and mortality in elderly patients with isolated systolic hypertension. The rate-lowering calcium antagonists can be used as alternatives to beta-blockers in patients with coronary artery disease and hypertension. Calcium antagonists can be used as alternatives to ACE inhibitors in patients with hypertension and concomitant diabetes mellitus and/or renal disease. Some dihydropyridine calcium antagonists may be useful as alternatives to ACE inhibitors in patients with hypertension and systolic heart failure. Calcium antagonists appear to be extremely useful in patients with cyclosporin-induced hypertension, and in patients with hypertension and concomitant Raynaud's phenomenon and/or migraine. The rate-lowering agents can be used in patients with atrial tachyarrhythmias and hypertension. Clinicians should be aware of drug-drug interactions involving calcium antagonists, especially after the recent problems with mibefradil. Although retrospective studies have caused controversy regarding the safety of calcium antagonists in patients with hypertension, recent prospective studies have revealed no major safety concerns with these drugs.
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PMID:How to use calcium antagonists in hypertension: putting the JNC-VI guidelines into practice. Joint National Committee for the Prevention, Detection, Evaluation and Treatment of High Blood Pressure. 1055 31

Bradykinin (BK) increased carotid blood flow (CBF) and jugular nitric oxide (NO) levels when administered into the common carotid artery of rabbits, and potentiated selectively, when infused together with histamine (HIST) or serotonin (5-HT), their effects on both CBF and jugular NO levels (but not vice versa). Such a potentiation was prevented and reversed only by nitroarginine or 1,10-phenanthroline (PHE) (which also reduced basal jugular NO levels) and did not involve the BK1 or BK2 receptors. Either HIST or 5-HT potentiated (likely involving the H1 and 5-HT2 receptors, respectively) the activating effect of BK on kininase I (K1), thus increasing the availability of L-arginine for the synthesis of NO. In patients with migraine, venous NO and K1 activity were higher during HIST desensitization than in basal conditions; moreover, HIST reduced the activities of prekallikrein (pre-KAL), kallikrein (KAL) and kininase II (K2) in the venous blood of these patients, in which the intensity of pain was related to the levels of plasma NO, and the administration into the humeral artery during circulatory arrest of BK alone (but not HIST) or BK and HIST together caused a strong pain attack. BK was confirmed to interact selectively with other autacoids in regulating systemic and local hemodynamics through the system of NO.
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PMID:Regulatory role of bradykinin in the coronary and cerebral circulations and in systemic hemodynamics. 1060 29


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