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 sympathectomy of the ear artery in rabbits on the activity of a number of redox coenzymes inthe vascular wall (lactic, glucose-6-phosphoric, isocitrate, and succinic dehydrogenases: LDH, G-6-PDHm isoCDH, and SDH, respectively) was studied by the quantitative histochemical method. Sympathectomy produced a significant diminution of all the dehydrogenase activities. The effect of adrenalin and noradrenaline on the dehydrogenase activities differed. Adrenalin increased thI LDH activity in the intact perfused artery, but had no effect on the CDH and G-6-PDH. Contrary to adrenalin, noradrenaline increased not only the LDH activity, but also that of the G-6-PDH. The action of noradrenaline on the sympathectomized vessel depended on the place of noadrenaline entrance, i.e. through the intima or the adventitia.
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PMID:[Effect of desympathization and catecholamines on metabolic processes in the rabbit otic artery]. 88 11

A case of severe and prolonged hypotension following intake of 10 mg enalapril in a patient with slight hyponatraemia is described. Despite administration of isotonic NaCl and treatment with dopamine infusion, it did not prove possible to maintain a stable blood pressure. Adrenaline and ephedrine were required intravenously on repeated occasions on account of symptom-producing hypotension with a systolic pressure as low as 60 mmHg. On account of the increasing use of ACE-inhibitors, it is recommended that the specific antidote, angiotension II, should be registered in Denmark and should be available in all hospitals.
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PMID:[Severe prolonged hypotension after the first dose of enalapril in a patient with essential hypertension]. 180 90

We examined the effect of angiotensin I (AI), without the effect of angiotensin II (AII) converted from AI, on the weight of the adrenal glands, adrenal corticosterone (B) and adrenal aldosterone under conditions where the renin-angiotensin system was suppressed, since a reduction in the size of the adrenal glands is often observed in DOCA/salt hypertensive rats. Sixty male Wistar rats fed on a 1% NaCl solution were divided into 6 groups as follows: a) Salt group: received sesame oil and vehicle, b) Salt + C group: received sesame oil and MK422 (0.14 mg/day), an angiotensin converting enzyme inhibitor (CEI), c) DOCA group: received DOCA (30 mg/week) and vehicle, d) DOCA + A group: received DOCA and AI (0.5 mg/kg/day), e) DOCA + A + C group: received DOCA and AI with MK422, and f) DOCA + C group: received DOCA and MK422. After 4 weeks, the rats were sacrificed to sample their blood and remove their adrenal glands. There was no significant difference in adrenal B among the groups apart from the DOCA + C group. Adrenal aldosterone was lower in the groups of DOCA/salt hypertensive rats than in the Salt group and Salt + C group. Furthermore, the DOCA + A + C group and DOCA + C group had lower adrenal aldosterone levels than the DOCA group and DOCA + A group.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Preventive effect of angiotensin I on weight reduction in the adrenal glands of DOCA/salt hypertensive rats. 208 30

SCH 33861 (7- N- 1(S)-(Carboxy)-3-phenylpropyl -(S)-alanyl 1,4-dithia-7-azaspiro 4.4 nonane-8(S)-carboxylic acid) is a novel, non-sulfhydryl angiotensin converting enzyme (ACE) inhibitor with marked topical ocular hypotensive activity. The present study evaluated the degree of systemic ACE inhibition resulting from topical administration of 0.01 and 0.1% concentrations (10 and 100-fold greater than needed to lower IOP) of SCH 33861 in conscious rabbits. For reference purposes, captopril, a prototype ACE inhibitor, was examined at concentrations 5 and 20-fold greater than needed to lower IOP. Neither 0.01 nor 0.1% topical SCH 33861 led to inhibition of pressor responses to 0.3 micrograms/kg iv challenges with angiotensin I (AI) over a 4 hr period. Captopril, in contrast, caused significant attenuation of AI pressor responses. The magnitude and duration of systemic ACE inhibition following captopril administration was concentration related. Intravenous administration of the same dose administered topically did not cause any systemic ACE inhibition with 0.01% SCH 33861. Following iv 0.1% SCH 33861, 0.5 or 2.0% captopril, AI responses were inhibited 60-70% indicating the ability to inhibit ACE if any systemic absorption took place. Topical administration of 0.01% SCH 33861 twice daily for five days also did not produce systemic ACE inhibition. These findings indicate that topical amounts of SCH 33861 greatly in excess of those needed to effect reductions in IOP have an exceptionally low potential for producing systemic effects.
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PMID:Systemic effects resulting from topical ocular administration of SCH 33861, a novel ACE inhibitor ocular hypotensive agent. 304 62

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)
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PMID:[Influence of angiotensin on the secretion of aldosterone in idiopathic hyperaldosteronism]. 311

Interaction between kininase II and anaesthesia is not well described. Twenty two patients treated by kininase II for congestive heart failure are studied during anaesthesia for cardiovascular surgery. A first group of seventeen homogeneous hemodynamic data are reported. High cardiac index contrasts with severe clinical cardiac failure. A second group of inhomogeneous patients are separately described. Vasoconstrictor can be codified in the situation of low systemic resistance with high cardiac index. Preoperative treatment can be continued, under requirement of hemodynamic monitoring.
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PMID:[Is it necessary to discontinue captopril before heart surgery?]. 355 42

The purpose of the present study was to evaluate the role of the renin-angiotensin system in the secretion of aldosterone during restriction of dietary sodium intake. Rats were kept on control or low-sodium diet for one week. On the 7th morning of diet osmotic minipumps filled with the angiotensin converting enzyme inhibitor (CEI) SQ 20,881, or empty pumps, were implanted subcutaneously (sc). The rats were sacrificed 23 h later. Peripheral blood was analyzed for hormones and electrolytes. Adrenal capsular tissue (z. glomerulosa) was incubated for the determination of the conversion of [3H]corticosterone to [3H]aldosterone. Sodium depletion had no effect on plasma sodium, but it increased potassium concentration. Infusion of CEI had no significant effect on plasma electrolytes. Plasma renin activity was increased both by sodium depletion and CEI. The mean serum aldosterone level was twelve times higher in sodium depleted animals than in controls. Aldosterone level was reduced by about 60 per cent in CEI-infused animals both on control and low-sodium diet. The conversion of corticosterone to aldosterone was significantly stimulated by sodium deprivation. This effect was also inhibited by the CEI SQ 20,881.
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PMID:Role of the renin-angiotensin system in the adaptation of aldosterone biosynthesis to sodium restriction in the rat. 615 22

In the pithed rat preparation captopril, enalapril, teprotide and saralasin given intravenously attenuated pressor responses to both spinal sympathetic nerve stimulation and exogenous noradrenaline, indicating that angiotensin has a potent adrenergic facilitating action. Bi-lateral nephrectomy abolished the effects of captopril on nerve stimulation but responses to noradrenaline were still inhibited following nephrectomy, indicating that part of the post-junctional actions of captopril might not be angiotensin dependent. Both phenylephrine and clonidine are also inhibited by captopril in the pithed rat. It is thus not clear whether captopril is interacting with post-junctional alpha 1- or alpha 2-adrenoceptors. Vasoconstrictor responses to nerve stimulation are greater in SHR than WKY and captopril is more effective at inhibiting responses in the SHR than it is in WKY. These interactions between captopril and the sympathetic nervous system could explain the effectiveness of ACE inhibitors as antihypertensive agents.
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PMID:Interference by inhibitors of the renin-angiotensin system with neurogenic vasoconstriction. 619 45

Phase I human studies can be used to differentiate a novel agent from existing drugs that influence the same pathway (eg, angiotensin-converting enzyme [ACE] inhibitors). Human forearm vasculature provides a useful experimental model for such studies because antagonism of local effects of agonists on resistance vasculature can be quantified, unconfounded by reflex cardiovascular responses to systemically applied agonists. In this model, inhibition of ACE with enalapril (given orally) or its active metabolite enalaprilat (given into the brachial artery) influences responses to some, but not all, vasoactive peptides that are substrates of ACE in vitro. Vasoconstrictor responses to angiotensin I (A I) are antagonized, while vasodilator responses to bradykinin are potentiated. Responses to vasoactive intestinal peptide (VIP), substance P (SP), and atrial natriuretic peptide (ANP) are unaltered by ACE inhibition. Vasodilator responses to bradykinin are antagonized by the B2-receptor icatibant and are blunted (but not abolished) by inhibition of the L-arginine/NO pathway with L-NG-monomethyl arginine. In contrast to inhibition of ACE with enalapril, blockade of the AT1 receptor with losartan results in similar inhibition of vasoconstrictor responses to both A I and angiotensin II but has no significant effect on the vasodilator action of bradykinin. The implication is that losartan provides more specific blockade of the renin-angiotensin pathway than does inhibition of ACE. The in vivo methods described in the study confirm the mechanistically relevant differentiation between AT1-receptor antagonism and ACE inhibition in humans.
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PMID:Angiotensin II-receptor (AT1) blockade in the human forearm. 891 43

Angioneurotic edema can involve the face and mucous membranes and can progress toward laryngeal obstruction and death. ACE inhibitors are the main etiology, followed by the hereditary forms and the acquired forms. Quantitative and qualitative measurements of C1 inhibitors are important to differentiate the common form of HAE from the variant form. Long-term therapy is based upon antifibrinolytics and androgen therapy. Fresh frozen plasma can be given for short-term therapy. Treatment of the acute attack is mainly supportive directed toward airway protection. Epinephrine, steroids, and antihistamine have not been proven to be efficacious.
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PMID:Angioneurotic edema. 905 26


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