Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P01185 (vasopressin)
 23,126 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We studied the activity of angiotensin I converting enzyme (ACE, kininase II, E.C. 3.4.15.1) in discrete areas of the brainstem and limbic system, and in circumventricular organs, pineal gland and choroid plexus of homozygous Brattleboro rats (DI) which are characterized by vasopressin deficiency and diabetes insipidus, with or without vasopressin replacement. We also determined ACE activity in heterozygous Brattleboro (HZ) and Long-Evans (LE) control rats. We found changes in ACE activity in several brain areas and the pineal gland of Brattleboro rats. ACE activity was increased in DI rats with respect to HZ and LE controls in the A1 area of the brainstem, locus coeruleus, and triangular nucleus of the septum. ACE activity in the A2 area of the brainstem, the nucleus tractus spinalis nervi trigeminii and the pineal gland was enhanced in both HZ and DI rats with respect to that of LE controls, but was not different between HZ and DI rats. ACE activity did not change in the other extrahypothalamic areas studied. The elevated ACE activity in extrahypothalamic areas of DI rats was not reversed by vasopressin replacement. These results suggest that a relationship between central vasopressin and angiotensin or bradykinin systems may exist in selective extrahypothalamic areas of the rat brain, and that peripherally administered vasopressin cannot influence this relationship.
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PMID:Selective increase of angiotensin-converting enzyme activity in discrete extrahypothalamic areas of Brattleboro rats. 631 41

Several components are responsible for circulatory control at the central, regional, and microcirculatory level. Angiotensin-converting enzyme (ACE) inhibitors are known to act beneficially on circulation by various mechanisms. The influence of continuous i.v. administration of the ACE inhibitor enalaprilat on regulators of circulation was studied in 45 critically ill patients. According to a prospective randomized sequence, either 0.25 mg/h (group 1, n = 15) or 0.5 mg/h (group 2, n = 15) of enalaprilat or saline solution as placebo (control group, n = 15) were continuously given. Infusion was started on the day of admission to the intensive care unit (ICU) and continued for the next 5 days. From arterial blood samples, plasma levels of endothelin-1 (ET), atrial natriuretic peptide (ANP), renin, vasopressin, angiotensin-II, and catecholamines (epinephrine, norepinephrine) were measured. All measurements were carried out before infusion (= baseline values) and during the next 5 days. In both enalaprilat groups, mean arterial blood pressure (MAP) decreased similarly; heart rate (HR) and central venous pressure (CVP) did not change, and were without differences in comparison to the untreated control. Except for ET, plasma levels of all vasoactive substances exceeded normal range at baseline. Angiotensin-II plasma concentrations significantly decreased during enalaprilat infusion (0.25 mg/h: from 53.1 +/- 11.3 to 22.1 +/- 9.3 pg/ml; 0.50 mg/h: 62.1 +/- 14.4 to 17.9 +/- 7.9 pg/ml), but they remained significantly elevated in the untreated control patients. Vasopressin plasma level increased only in the control group (p < 0.01) and decreased in the patients in whom 0.50 mg/h of enalaprilat was infused.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Continuous i.v. administration of the angiotensin-converting enzyme inhibitor enalaprilat in the critically ill: effects on regulators of circulatory homeostasis. 776 7

A survey is given of the currently used therapeutics in the treatment of chronic congestive heart failure. Symptomatic treatment is usually performed along the following lines: rest, sodium and fluid restriction to unload the decompensating heart, loop diuretics, angiotensin-converting enzyme inhibitors or other vasodilators; inotropic agents to improve the heart's mechanical performance; attempts to counteract the neuro-endocrine compensatory mechanisms, that is the activated sympathetic nervous and renin-angiotensin-aldosterone systems, as well as the rise in vasopressine levels. New insights have been obtained in the effects of cardiac glycosides, which are probably rather based on counteracting the elevated sympathetic neuronal activity than on their weak and uncertain inotropic action. Angiotensin-converting enzyme inhibitors are probably more effective than classical vasodilators owing to their additional interaction with the neuro-endocrine compensatory mechanisms. Ibopamine, a prodrug of epinine, appears to be rather a vasodilator and antagonist of the neuro-endocrine compensatory mechanisms than an inotropic agent. The most important clinical trials addressing the efficacy and adverse reactions to the various aforementioned therapeutics are discussed. New, experimental approaches in the drug treatment of chronic congestive heart failure include beta-blockers, calcium antagonists, vasopressin antagonists and inhibitors of atrial natriuretic peptide degradation.
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PMID:Pharmacotherapy of congestive heart failure. Currently used and experimental drugs. 788 21

Ventricular failure is accompanied by a series of neurohormonal responses that result in vasoconstriction. Vasoconstriction develops and is mediated by norepinephrine, angiotensin II, and vasopressin. Vasoconstriction maintains blood pressure but contributes to deterioration in ventricular function. Baroreceptor dysfunction contributes to the syndrome by failing to ameliorate the sympathetic overstimulation. Drug therapy has historically included positive inotropes until recent data suggested that these drugs contributed to worsened survival. The role of digitalis glycosides in patients with ventricular failure who are in normal sinus rhythm remains a subject of scrutiny. Thus far, no long-term oral positive inotrope has replaced digoxin. Vasodilator therapy and interference with the neurohormonal response have become the major approaches to pharmacologic management of ventricular failure. Angiotensin-converting enzyme inhibitors have shown convincingly that they improve survival, slow the course of disease progression, and block the neurohormonal response to ventricular failure. New treatments for ventricular failure must be directed at long-term gain rather than short-term hemodynamic results.
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PMID:Neurohormonal response to ventricular failure: pharmacologic management. 810 97

Angiotensin-converting enzyme inhibitors improve long-term survival in patients with left ventricular dysfunction after a myocardial infarction, but their mechanism of action is not entirely clear. The neurohormonal effects may be important in this respect, as well as an early hemodynamic unloading induced by these drugs. The primary objective was to assess the effect of trandolapril on plasma levels of atrial natriuretic peptide. A secondary objective was to assess the effects of trandolapril on selected neurohormones, vasoactive peptides and enzymes, which may be important in the development of left ventricular remodeling and heart failure following an acute myocardial infarction. A total of 119 patients with an acute myocardial infarction and a wall motion index < or =1.2 (16-segment echocardiographic model) were randomized to double blind treatment with trandolapril or placebo within 3-7 days after the onset of infarction. Blind treatment was discontinued 21 days after the index infarction. Venous blood samples were collected at rest, before randomization and on the day after treatment was discontinued. At the end of the study, there were no differences in plasma levels of atrial natriuretic peptide between the two treatment groups. Angiotensin-converting enzyme activity was suppressed and plasma renin activity was higher in the trandolapril group. No differences in plasma levels of N-terminal pro-atrial natriuretic peptide, brain natriuretic peptide, aldosterone, noradrenaline, adrenaline, vasopressin, big endothelin-1 and neuropeptide Y were found between the two treatment groups. There were positive correlations between several markers of neurohormonal activation at baseline and variables expressing left ventricular dysfunction and clinical heart failure. Neurohormonal activation is related to left ventricular dysfunction. The effects of 2-3 weeks of angiotensin-converting enzyme inhibition on neurohormonal activation does not predict the already established beneficial long-term effects after myocardial infarction. Thus, early modulation of circulatory neurohormone levels may not be a major mechanism for the efficacy of angiotensin-converting enzyme inhibitors in these patients. Selected plasma hormone markers may still be used to identify patients who might get the greatest benefit from treatment.
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PMID:Early neurohormonal effects of trandolapril in patients with left ventricular dysfunction and a recent acute myocardial infarction: a double-blind, randomized, placebo-controlled multicentre study. 1116 38

The objective was to investigate whether the renin-angiotensin (RA) system and related peptides endothelin-1 (ET-1) and vasopressin (VP) influence the development of coronary artery disease (CAD). Angiotensin I-converting enzyme (ACE) insertion/deletion (I/D) gene polymorphism has been associated with the risk of CAD. The ACE I/D polymorphism determines ACE activity, but plasma levels of other RA system components remain unchanged. However, ET-1 and VP production could be increased by RA system-dependent stimulation, continually promoted by paracrine stimulation and sustained by neointimal growth. ET-1 and VP have not been associated with the ACE I/D polymorphism so far. The present study investigated the association of the ACE I/D polymorphism with plasma concentrations of ET-1 and VP, as well as with renin, angiotensin-II (AT-II) and ACE activity in 98 Caucasian individuals with CAD. ACE I/D polymorphism showed no association with plasma levels of VP, ET-1, AT-II or renin. These parameters were also not associated taking into consideration different patient variables, such as diabetes mellitus, hypertension or severity of CAD. Only plasma ACE activity was associated with the D allele. In conclusion, the ACE I/D polymorphism could not be related to plasma concentrations of VP, ET-1, renin or AT-II, but as previously demonstrated, it could only be related to ACE activity in patients with CAD. Differences in ACE activity between ACE I/D genotype subgroups are probably compensated within the RA system itself or within non-ACE pathways, so that plasma concentrations of the related peptides ET-1 and VP remain unaffected.
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PMID:Endothelin-1 and vasopressin plasma levels are not associated with the insertion/deletion polymorphism of the human angiotensin I-converting enzyme gene in patients with coronary artery disease. 1257 92

Angiotensin-converting enzyme (ACE) inhibitors inhibit the enzyme that cleaves angiotensin I to form angiotensin II. They are potent vasodilators as they decrease concentrations of angiotensin II and noradrenaline and increase concentrations of bradykinin and nitric oxide. They reduce secretion of aldosterone and antidiuretic hormone, thus reducing salt and water reabsorption by the kidney (Groban and Butterworth, 2006).
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PMID:Angiotensin-converting enzyme inhibitors in the perioperative period. 2250 63

Angiotensin-converting enzyme inhibitors (ACEI's) are an important medication in the treatment of congestive heart failure. However, ACEIs may cause harmful side effects, such as the syndrome of inappropriate secretion of antidiuretic hormone (SIADH), which is a rare but important side effect. We describe here a case of SIADH associated with ACEI administration in a 6-year-old boy with restrictive cardiomyopathy. After recovery from acute exacerbation of congestive heart failure by tolvaptan administration, an ACEI (cilazapril) was started to decrease the production of angiotensin II, which upregulates serum antidiuretic hormone secretion. The patient's heart failure symptoms worsened, including accumulation of right pleural effusion and ascites, after the initiation of ACEI administration. Cessation of ACEI administration dramatically improved his symptoms. Because it is difficult to distinguish SIADH associated with ACEI from worsening congestive heart failure, the possibility of fluid retention due to ACEI administration should always be considered when this agent is administered to patients with heart failure.
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PMID:Syndrome of inappropriate secretion of antidiuretic hormone associated with angiotensin-converting enzyme inhibitor administration. 2262 87


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