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)

Catopril, an inhibitor of angiotensin converting enzyme, was given orally during cardiac catheterisation to 6 normotensive patients with refractory congestive heart-failure. 60--180 minutes after administration of 25 mg captopril, arterial pressure fell by 25%, cardiac index rose by 38%, and left-ventricular pressure and right-atrial pressure fell by 25% and 40% respectively. Plasma-renin activity rose while plasma noradrenaline and aldosterone fell. These data suggest that, in the short term, captopril can reduce both preload and afterload, and improve cardiac function, in refractory congestive heart-failure.
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PMID:Improvement of chronic congestive heart-failure by oral captopril. 8 79

The activity of the glycolytic enzymes and of the glucose-6-phosphate dehydrogenase (G-6-PDH) were compared with the content of noradrenaline in rat myocardium and the liver after the intraperitoneal injection of high doses of noradrenaline. It was shown that 24 hours after int noradrenaline injection which caused exhaustion of endogenous catecholamine supply, the lactate content and the activities of lactic dehydrogenase were increased in the myocardium; the activity of hexokinase and G-6-PDH in rat myocardium and the liver were also increased, whereas the glucokinase activity was decreased. In these experiments alterations of the enzyme activities were shown to be similar to the alterations in the dystrophic tissues in which the catecholamine content was sharply decreased. The role of the sympathetic nervous system and its mediators in the mechanism of the enzyme regulation of the energy metabolism in the myocardium and the liver is discussed.
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PMID:[Activity of energy metabolism related enzymes in the myocardium and liver following administration of large doses of noradrenaline]. 17 88

1 The vascular bed of the tongue in situ was perfused with blood through the lingual arteries at a constant pressure in anaesthetized dogs. All drugs except for SQ 14,225 were administered intra-arterially.2 Prostaglandin F(2alpha) (PGF(2alpha)) produced a dose-dependent increase in blood flow through the lingual arteries (vasodilatation).3 Marked desensitization was observed on the vasodilator responses to repeated administration of PGF(2alpha).4 The vasodilator response to PGF(2alpha) was abolished by tetrodotoxin in doses that abolished the vasodilator response to electrical stimulation of the lingual nerve.5 The vasodilator response to PGF(2alpha) was not affected by hexamethonium in doses that almost abolished the vasodilator response to lingual nerve stimulation.6 The vasodilator responses to PGF(2alpha) and to lingual nerve stimulation were scarcely modified by (-)-hyoscyamine in doses that fully antagonized the vasodilator response to acetylcholine.7 Electrical stimulation of the vago-sympathetic trunk and noradrenaline produced a decrease in blood flow through the lingual arteries.8 These results indicate that the vasodilator response of the tongue to PGF(2alpha) is due exclusively to excitation of parasympathetic postganglionic neurones and that neuronal receptors involved are quite distinct from nicotinic receptors.9 Intravenous administration of SQ 14,225, an inhibitor of angiotensin I converting enzyme or kininase II, augmented the vasodilator responses to bradykinin and kallikrein but not that to lingual nerve stimulation.10 The results suggest that neither kallikrein nor*kinin (including bradykinin) is responsible for the parasympathetically induced vasodilatation in the tongue.
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PMID:Vasodilatation by prostaglandin F2alpha in the canine tongue through a parasympathetic mechanism. 66 1

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 3-hour electrostimulation of the aortic arch in rabbits was followed by the exhastion of the tissue noradrenaline stores in the myocardium accompanied by increase in the activity of the glycolysis enzymes and of the enzyme limiting the process of the pentosophosphate route-G-6-PDH. The use of noradrenaline precursor - 1-DOPA restored the noradrenaline level in the myocardium completely after a 48-hour stimulation. Simultaneously there were noted no changes in the activity of the enzymes under study caused by the stimulation of the aortic arch. The data obtained confirmed the important role of the sympathetic nervous system and of its mediator - noradrenaline in the mechanism of the tissue metabolism regulation, whose derangement played a significant role in the development of dystrophic lesions of the heart tissue.
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PMID:[Activity of various enzymes of energy metabolism of the myocardium after neurogenic injury]. 102 3

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.
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PMID:Humoral response and blood pressure regulation during hypercapnia and haemorrhage in dogs. 107 98

The relationship between experimental magnesium deficiency and blood pressure is complex and still the subject of much debate. The effect of Mg deficiency and blood pressure in Wistar rats receiving a Mg deficient diet (0.080 g/kg) for 40 weeks was examined. Deficient rats, when compared to controls, showed an initial transitory phase of hypotension, followed by normalization of blood pressure and then hypertension beginning after 15 weeks on the deficient diet. During the whole experimental period, heart rate was significantly increased in deficient rats as compared to controls. The fact that hypotension resulting from Mg deficiency of short duration can be inhibited by antihistamines and by indomethacin suggests that various mediators seen during the inflammatory period of Mg deficiency could be involved. Mg deficiency of long duration was accompanied by hypertension. When Mg-deficient rats received the control diet for a period of 3 weeks, Mg supplementation only partially corrected the hypertension. The hypertension was not a consequence of stimulation of the renin-angiotensin system since the plasma renin activity was not modified and ACE activity was reduced. These deficient rats showed a significantly lower vasopressor response to noradrenaline than control rats. Several factors such as increase in collagen, changes in elastin and arterial elasticity, total lipid content, and calcifications may account for the hyporesponsiveness to contractile agonists.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Magnesium and blood pressure. I. Animal studies. 139 7

The pressor responsiveness to noradrenaline was assessed before and after four weeks of treatment with enalapril (20 mg/day) in eight mild-to-moderate essential hypertensives, in eight normotensive type II diabetics and in eight mild-to-moderate hypertensive type II diabetic patients. The ACE inhibitor interfered to the same extent with the renin-angiotensin system and did not alter noradrenaline kinetics in the three groups of patients, but significantly reduced the arterial responsiveness only in non-diabetic subjects. It is suggested that factors, such as an exaggerated sodium retention, might determine the lack of effect of enalapril in diabetic patients.
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PMID:ACE inhibition in diabetic patients: effect on pressor responsiveness to noradrenaline. 143 67

We assessed blood pressure and neurohumoral factors at rest and during exercise in 10 patients with essential hypertension before and after treatment with the new angiotensin converting enzyme inhibitor, alacepril (25-50 mg day-1). Alacepril significantly lowered mean blood pressure at rest and at the same exercise load as before treatment without affecting heart rate response. The response of plasma renin activity, plasma aldosterone, and plasma adrenaline were not changed by alacepril, but increase of plasma angiotensin II and plasma noradrenaline during exercise were significantly attenuated after alacepril treatment (ANOVA, P = 0.04, both). The change in mean blood pressure during exercise was positively correlated with the decrease in plasma angiotensin II (r = 0.65, P < 0.05). These results demonstrated that alacepril was effective in essential hypertension both at rest and during exercise, suggesting that the antihypertensive effect during exercise might be related to the decrease in pressor hormones, especially in plasma angiotensin II.
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PMID:Effect of alacepril on blood pressure and neurohumoral factors at rest and during dynamic exercise in patients with essential hypertension. 145 72

Since converting enzyme and kininase II are identical enzymes and probably influences both, the biosynthesis of Ang II and the metabolism of bradykinin we investigated the effects of bradykinin, desArg-bradykinin and some bradykinin antagonists (desArg[9]-Leu[8]-bradykinin, HOE S 890307) on the sympathetic outflow of pithed SHR or Brown-Norway-Rats before and after acute or chronic inhibition of the converting enzyme by ramipril. bradykinin increased dose dependently the noradrenaline and adrenaline release in particular when the converting enzyme was inhibited. DesArg-bradykinin caused a dose-dependent increase in adrenaline release only after converting enzyme inhibition. The bradykinin-antagonists led to an increase in adrenaline release during ramipril administration. The weak but significant stimulation of adrenaline release by the bradykinin antagonists after converting enzyme inhibition might be due to unspecific actions on the adrenal medulla possibly induced by histamine release from mast cells.
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PMID:Modulation of presynaptic sympathetic activity by kinins and related compounds: influence of converting enzyme inhibition. 146 84


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