Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020538 (hypertension)
170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The present study was designed to clarify the role of serum angiotensin I-converting enzyme (ACE) in the occurrence and maintenance of hypertension in essential hypertension (EH). For this purpose, following experiments were carried out: 1) Correlations between serum ACE activity and renin activity (PRA), aldosterone concentration (PAC) and bradykinin concentration (PBC) in plasma, and blood pressure (BP) as well as serum creatinine levels. 2) Circadian rhythm of serum ACE activity. and 3) Effect of furosemide, upright posture, both furosemide and upright posture, propranolol, indomethacin, 9 alpha-fluorocortisol or angiotensin II (A-II) on the serum ACE activity, PRA, PAC and circulating plasma volume (CPV). The following results were obtained: The serum ACE activity was 30.2 +/- 5.0 U/ml (means +/- SD) in EH as a group, which was significantly higher than that (27.3 +/- 3.9 U/ml) in age matched normotensive subjects (NT) (p less than 0.001). While there was no significant difference in the enzyme activity between low-renin EH (LREH) and NT, a significant difference was found between normal- (NREH) or high-renin EH (NREH) and NT (p less than 0.05 for NREH, p less than 0.01 for HREH). A negative correlation was observed between enzyme activity and age in EH (r = -0.221, 0.05 less than p less than 0.10) as well as in NT (r = -0.306, p less than 0.05). No significant relationships were observed between enzyme activity and BP in either EH or NT. There was a significant positive correlation between enzyme activity and PRA in NT. (r = 0.501, p less than 0.001), NREH (r = 0.658, p less than 0.001) and HREH (r = 0.695, p less than 0.001). However, no significant relationship was found between them in LREH. The enzyme activity was significantly correlated to PAC in NT (r = 0.368, p less than 0.01), NREH (r = 0.567, p less than 0.001) and HREH (r = 0.529, p less than 0.01), but not in LREH. Although no significant correlation was observed between enzyme activity and PBC in NT, NREH and HREH, a significant relationship was found in LREH (r = -0.460, 0.05 less than p less than 0.10). The enzyme activity was not related to serum creatinine levels in EH as well as in NT. In NT, the serum levels of ACE activity reached a maximum values at 6:00 a.m. or 9:00 a.m., and gradually decreased between 6:00 p.m. and 3:00 a.m. An almost similar circadian rhythm of enzyme activity was found in EH.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Clinical significance of serum angiotensin I-converting enzyme in essential hypertension]. 300 63

Angiotensin-converting enzyme (ACE) inhibitors are a new class of drugs, whose main indications are the treatment of hypertension and of heart failure. Data obtained with captopril, the first orally active ACE inhibitor, affords an understanding of the rationale of their therapeutic use based on the knowledge of their mechanisms of action, efficacy, contraindications and precautions, dosage and frequency of administration, side-effects, interactions and advantages. ACE inhibitors appear to exert their haemodynamic effect mainly by inhibiting the renin-angiotensin-aldosterone system, but also by modulating sympathetic nervous system activity and by increasing prostaglandin synthesis. Therefore they act both on vasoconstrictor and volume factors, since they cause vasodilation (the main effect) and mild natriuresis without affecting the heart rate and contractility and, probably, favourably influencing renal, coronary and cerebral circulation. So far it appears that ACE inhibitors can be usefully employed in the treatment of heart failure, in which they reduce both pre- and after-load, and mainly of hypertension. In the past captopril has been used to treat only severe and or resistant hypertension and some secondary forms, like renal parenchymal and renovascular hypertension, but now it seems that captopril is useful also to treat mild to moderate essential hypertension. Their efficacy in reducing blood pressure is similar to that of thiazide diuretics and of beta-blockers, the two drugs now considered of first choice and they exert their hypotensive action without the development of pseudotolerance or tolerance. ACE inhibitors seem, at the moment, contraindicated in pregnancy and in hyperkalaemic syndromes and must be used with caution in patients with collagen disease (mainly associated with renal failure), with severe bilateral renal artery stenosis (and with severe artery stenosis of a solitary kidney) and with severe sodium depletion. It is now established that captopril has a flat dose response curve and that it must be given (twice daily) at a dose not exceeding 150 mg/day. The same pharmacological approach must be used with future ACE inhibitors in order to establish the right posology and the frequency of administration. In this respect enalapril seems to be a promising ACE inhibitor with a prolonged action (at least 24 hours). The exact posology of ACE inhibitors might be crucial, since it has been shown that the side-effects of captopril (skin rashes, fever, taste disturbances, proteinuria and neutropenia) are dose dependent.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Angiotensin-converting enzyme inhibitors in hypertension: a review. 300 82

Angiotensin-converting enzyme, the polypeptide that converts angiotensin I to angiotensin II, was measured in the serum of 114 pregnant women who had normal blood pressure, pregnancy-induced hypertension-preeclampsia, and chronic hypertension with or without pregnancy-induced hypertension. Angiotensin-converting enzyme levels were unrelated to weeks of gestation. The angiotensin-converting enzyme levels were similar in normotensive women (21.1 +/- 6.9 units/ml), women with chronic hypertension without pregnancy-induced hypertension (23.1 +/- 2.7 units/ml), and patients with pregnancy-induced hypertension where magnesium sulfate (22.6 +/- 8.7 units/ml) had been administered prior to angiotensin-converting enzyme assay, but these values were significantly less than those in patients with pregnancy-induced hypertension with no magnesium sulfate (29.1 +/- 6.5 units/ml) therapy and in women with chronic hypertension with superimposed pregnancy-induced hypertension (30.7 +/- 4.4 units/ml) (p less than 0.005). Maternal venous and umbilical venous and arterial angiotensin-converting enzyme levels were as follows: The maternal venous level was less than the cord venous level and greater than the cord arterial value. Neither neonatal size nor twin gestation influenced the angiotensin-converting enzyme levels. Patients with diabetes mellitus had variable angiotensin-converting enzyme values regardless of the status of the blood pressure. The physiologic theories of blood pressure control in pregnant women are discussed in relation to the renin-angiotensin, bradykinin, and prostaglandin systems.
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PMID:The relation of angiotensin-converting enzyme to the pregnancy-induced hypertension-preeclampsia syndrome. 300 58

A patient with secondary (sporadic type) hypokalemic periodic paralysis with relative hypertension had reninism with a high concentration of plasma angiotensin I (ANG-I) but no hyperaldosteronism or high angiotensin II value. Angiotensin-converting enzyme (ACE) activity was usually normal. Results of other hormonal analyses were also normal. However, the glomerular filtration rate and filtration fraction of the kidneys were greatly elevated. Despite severe hypokalemia, the patient's potassium clearance was high. No evidence of distinct hyperplasia of the juxtaglomerular cells was obtained. These results suggest that decreased affinity of ACE to the substrate ANG-I (so-called ACE dysfunction syndrome) produced the reninism and high concentration of plasma ANG-I, and that the latter induced an increase in the glomerular filtration rate of the kidneys with sequential occurrence of secondary hypokalemic periodic paralysis.
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PMID:Angiotensin I level and sporadic hypokalemic periodic paralysis. 302 Oct 78

Angiotensin-converting enzyme inhibitors are gaining acceptance as safe and effective agents for treatment of hypertension. Data on their use specifically in elderly hypertensives, however, are limited. Addressed in this review of the available literature are the questions whether they are effective hypotensives in the elderly, whether their effects are age-related, and what effects, if any, do they have on morbidity and mortality in geriatric hypertension.
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PMID:ACE-inhibitors in the treatment of elderly hypertensives. 303 39

Angiotensin-converting enzyme is a peptidase involved in the formation of angiotensin II and the inactivation of bradykinin. In a previous study we found elevated angiotensin-converting enzyme activity in women with pregnancy-induced hypertension prior to magnesium sulfate therapy and lower levels during therapy. This prospective study was undertaken in order to determine if angiotensin-converting enzyme activity indeed decreased after magnesium sulfate therapy. Sixteen patients with pregnancy-induced hypertension were studied before and during magnesium sulfate therapy. Angiotensin-converting enzyme activity was found to decrease 1 to 8 hours into therapy and then plateau between 9 and 24 hours. Possible mechanisms for this observation are discussed.
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PMID:Angiotensin-converting enzyme activity in hypertensive subjects after magnesium sulfate therapy. 303 26

Angiotensin converting enzyme (ACE, Kininase II, E.C. 3.4.15.1) activity was measured in the cerebrospinal fluid of 4- and 16-week-old spontaneously hypertensive rats (SHR) and age-matched Wistar-Kyoto (WKY) normotensive controls. Adult SHR showed higher cerebrospinal fluid enzyme activity than normotensive age-matched WKY (19.6 +/- 1 and 32.3 +/- 5 nmol/h per ml in WKY and SHR, respectively, P less than 0.025). Conversely, there were no significant differences in enzyme activity in the cerebrospinal fluid of young animals. Our results support the hypothesis of enhanced activity of the central angiotensin system during the established phase of spontaneous hypertension in rats.
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PMID:High angiotensin converting enzyme (kininase II) activity in the cerebrospinal fluid of spontaneously hypertensive adult rats. 303 95

Thirteen subjects with documented renovascular hypertension receiving chronic (greater than 1 month) therapy with an angiotensin-converting enzyme inhibitor (enalapril or captopril) underwent total and split renal function studies. Total glomerular filtration rate as assessed by inulin clearance was similar to that determined by radionuclide technique. Total effective renal plasma flow as assessed by p-aminohippurate clearance was lower than that determined by radionuclide technique. The glomerular filtration rate and effective renal plasma flow assessed by radionuclide technique of the stenotic kidney was comparatively lower than that of the non-stenotic kidney. No subject demonstrated complete loss of filtration or perfusion of the stenotic kidney. Five of six patients studied prospectively for 2 years have demonstrated stability of total renal function; the sixth patient, having a functional solitary stenotic kidney, has demonstrated stability of function following an initial abrupt decline in glomerular filtration rate and effective renal plasma flow. These results suggest that chronic angiotensin-converting enzyme inhibition therapy is not generally associated with near total absence of filtration of the stenotic kidney as has been suggested previously. Angiotensin-converting enzyme inhibitors may be safely and effectively utilized in the treatment of renovascular hypertension.
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PMID:Total and split renal function in patients with renovascular hypertension: effects of angiotensin-converting enzyme inhibition. 303 75

Angiotensin-converting enzyme inhibitors are potent vasodilators acting by inhibition of production of the vasoconstrictor angiotensin II. In adults, they are used for treatment of systemic hypertension and congestive heart failure and investigated for treatment of primary pulmonary hypertension. In infants and children, saralasin and captopril were found to be useful in treatment of systemic arterial hypertension, especially when associated with high plasma renin activity. Captopril has failed in the treatment of congestive heart failure associated with complex congenital heart diseases and in most cases of primary pulmonary hypertension. It has a clear beneficial effect in coarctation of the aorta and may have such an effect in endomyocardial diseases and ventricular septal defect. In adults, serious side effects have limited the use of captopril. New converting enzyme inhibitors, devoid of a sulfhydryl group, are expected to have a better safety profile.
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PMID:Cardiovascular drugs in children: angiotensin-converting enzyme inhibitors. 304 87

Mild hypertension accounts for approximately 60% of the mortality associated with high blood pressure. In addition to hypertension, other major cardiovascular risk factors include left ventricular hypertrophy (LVH), dyslipoproteinemia, and glucose intolerance. Thus, the effects of agents used to treat hypertension on these risk factors are of considerable importance. Large therapeutic intervention trials have shown that while adequate treatment of mild hypertension significantly and consistently reduces all-cause mortality as well as the risk of stroke and congestive heart failure, an anticipated reduction in coronary heart disease (CHD) has not been demonstrated. It is possible adverse metabolic side effects (hypercholesterolemia, hyperglycemia, hypokalemia) of widely used agents, such as diuretics and beta-blockers may be partially offsetting the beneficial effects of blood pressure reduction, with the net result being a failure of these agents to reduce the risk of CHD. Angiotensin-converting enzyme inhibitors (ACEIs) and calcium channel blockers do not produce these adverse metabolic derangements. The use of antihypertensive agents that have favorable or neutral metabolic effects should further reduce the risk of cardiovascular morbidity and mortality attributable to high blood pressure, including CHD.
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PMID:Beyond blood pressure control. Effect of antihypertensive therapy on cardiovascular risk factors. 305 46


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