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)

The relationship between plasma atrial natriuretic peptide (ANP) and plasma renin activity (PRA) was examined in patients with stable chronic obstructive pulmonary disease (COPD, n = 17). The plasma ANP level in patients was approximately twice that in normal subjects. A reciprocal relationship between ANP and PRA was shown in normal subjects; however, this relationship was not observed in COPD. Plasma ANP levels inversely correlated with PaO2, and tended to inversely correlate with angiotensin converting enzyme activity in serum. These results demonstrate that patients with COPD have higher plasma ANP concentration, and that ANP and PRA are not reciprocally related in stable COPD.
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PMID:[Atrial natriuretic peptide and plasma renin activity in patients with stable chronic obstructive pulmonary disease]. 138 34

First-dose-response of captopril 1 x 25 mg (no prodrug) and ramipril 1 x 2.5 mg (prodrug) were compared in two groups of 17 patients with moderate or severe hypertension and stimulated renin-angiotensin system (because of continuous diuretic therapy) by means of 24-h blood-pressure measurement at the 1st and 7th day of therapy. In the ramipril-group the antihypertensive effect started after 2 h, had its maximum (mean: -13/-8 mmHg) after 4 h and remained unchanged for 8 h. The antihypertensive effect was significant for 24 h. There was a slightly but not significant improved blood-pressure reduction at the 7th day compared to the 1st. The captopril-group showed a fast and marked decrease of blood pressure within the first hour, and reached its maximum (mean: -18/-10 mmHg) after 2 h. After 7 h there was no antihypertensive effect detectable. At the 7th day blood-pressure reduction was less pronounced compared to the 1st day. The results show that initial decrease of blood pressure in risk-patients is less severe with prodrug-ACE-inhibitors with slow onset of action so that counterregulation can be activated and prevent severe, fast, ACE-inhibitor-induced hypotension. 24-h-blood-pressure measurement is a sufficient method to evaluate first-dose-response of ACE-inhibitors.
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PMID:[Long-term blood pressure measurement for evaluating the first dose response of captopril and ramipril in patients with a stimulated renin system]. 138

In elderly hypertensive patients effect of antihypertensive treatment with Ca antagonist or ACE inhibitor on the heart were examined. Twenty-four elderly hypertensive patients with cardiac hypertrophy, aged 65-79 years old (mean +/- SEM, 71 +/- 1) were treated with Ca antagonist (nifedipine or nicardipine) or ACE inhibitor (captopril or enalapril) for 3 months. Thirteen patients had essential hypertension (EH: SBP greater than or equal to 160 mmHg and DBP greater than or equal to 95 mmHg, 70 +/- 1 years) and 11 had isolated systolic hypertension (ISH: SBP greater than or equal to 160 mmHg and DBP less than 95 mmHg, 74 +/- 2 years). Blood pressure (BP) and heart rate were measured every two weeks. In all patients, M-mode echocardiography was performed to measure left ventricular mass index (LVMI) and ejection fraction (EF), and the sympathetic nervous (plasma norepinephrine and epinephrine) and the renin-angiotensin system (plasma renin activity and aldosterone concentration), were assessed before and after 3 months of treatment. BP significantly decreased from 174 +/- 3/97 +/- 1 to 149 +/- 4/84 +/- 2 mmHg in EH and from 167 +/- 3/82 +/- 2 to 144 +/- 4/74 +/- 2 mmHg in ISH. LVMI was significantly reduced from 204 +/- 14 to 174 +/- 16 g/m2 in EH and from 179 +/- 14 to 156 +/- 12 g/m2 in ISH. EF showed no significant changes in either group. In ISH, the change in LVMI was significantly correlated with the change in systolic BP (r = 0.74, p less than 0.05). In EH, there was no significant relation between BP and LVMI changes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Effect of antihypertensive treatment in elderly hypertensive patients with cardiac hypertrophy]. 138 12

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

1. Certain genes drive the blood pressure of young spontaneously hypertensive rats (SHR) to stable hypertensive levels in adulthood. 2. Relatively brief blockade of the renin-angiotensin system in young SHR can reset the track of SHR pressure to a lower level for the life of the animal. This effect appears to be a characteristic of the SHR strain. 3. It is proposed that the expression of a particular SHR hypertensive gene depends on angiotensin and is limited to young animals. This hypothesis explains some of the phenotypic abnormalities observed in young SHR and the decremental long-term blood pressure effects following ACE inhibitor treatment. 4. The identity of the gene is unclear, but information from biochemical, physiological and pharmacological studies may direct attention to distinct candidate genes within specific chromosomal regions of interest. 5. Understanding these genetic mechanisms may have important implications for future preventive strategies.
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PMID:A developmental genetic mechanism involving angiotensin in spontaneously hypertensive rats. 139 12

Congestive heart failure is a syndrome common in the United States, especially in elderly patients. The most common etiology is coronary artery disease. A number of general factors contribute to the heart failure syndrome, including loss of muscle, decreased myocardial contractility, pressure or volume overload, or restricted filling. All of these factors may play a role in a given patient as, for example, with coronary artery disease. Although systolic dysfunction with a reduced ejection fraction is the most common heart failure syndrome, up to 40% of patients may have a relatively preserved ejection fraction with diastolic dysfunction. As the heart begins to fail, a number of compensatory mechanisms are activated. These include increased heart rate, the Frank-Starling mechanism, increased catecholamines, activation of the renin-angiotensin system, and release of atrial natriuretic peptides. Although these mechanisms are initially helpful to the cardiovascular system, they frequently overshoot, initiating a vicious cycle. For example, with a decrease in cardiac output, there is a reflex increase in systemic vascular resistance in order to maintain perfusion pressure. This increase in resistance, however, acts as a load on the left ventricle and further reduces cardiac output. The best evidence for the existence of this vicious cycle is the beneficial change in hemodynamics produced by vasodilator drugs and the ACE inhibitors. Thus, an understanding of pathophysiology allows for the selection of rational therapy. An unresolved problem in heart failure patients is how best to reduce the high incidence of sudden death, which is one of the major challenges for the future.
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PMID:Pathophysiology of congestive heart failure. 139 15

Angiotensin-converting enzyme inhibition with enalapril increases the number of glomeruli with juxtaglomerular cells and the number of cells in the afferent arteriole that express the renin gene and contain renin. However, renin release from these newly recruited renin-containing cells has not been demonstrated. Sodium depletion also has been shown to increase renal renin messenger RNA levels. The aim of these studies was to determine whether increases in renin secretion are a result of altered numbers of cells synthesizing/releasing renin or a change in the amount of renin release per cell, or both. Adult Wistar-Kyoto rats were treated with enalapril or sodium depleted and single cell renin secretion of enzymatically dispersed renal cortical cells was examined by reverse hemolytic plaque assay. Enalapril treatment increased the number of renin secreting cells by approximately 10-fold (P < 0.05). The newly recruited renin-secreting cells were not responsive to changes in extracellular calcium concentration or the presence of isoproterenol. At physiological (2.5 mM) extracellular calcium concentration, the amount of renin secreted per cell was approximately 2-fold greater (P < 0.05) when cells from enalapril-treated rats were compared to controls and sodium depletion increased both the number of renin-secreting cells and the amount of renin secreted by approximately 35% (P < 0.05). Angiotensin II (AII) inhibited the number of cells secreting renin in cortical cells prepared from enalapril-treated and control rats. In conclusion, angiotensin converting enzyme inhibition increased renin secretion predominantly by recruitment of additional renin-secreting cells and, to a lesser extent, by augmentation of the amount of renin released per cell. In contrast, sodium depletion increased renin secretion equally by both mechanisms. Newly recruited renin-secreting cells were not regulated by the extracellular calcium concentration or beta-adrenergic stimulation. Angiotensin II inhibited renin secretion directly by decreasing the number of individual cells releasing renin through a process which was independent of the extracellular calcium concentration.
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PMID:Effects of angiotensin converting enzyme inhibition, sodium depletion, calcium, isoproterenol, and angiotensin II on renin secretion by individual renocortical cells. 139 4

The cardiac interstitium is composed of non-myocyte cells and a structural fibrillar protein network which plays a dominant role in governing the structure, architecture, and mechanical behaviour of the myocardium. Herein we review the fibrillar collagen network, its various components, and the functions they serve in the normal and structurally remodelled myocardium in arterial hypertension. The heterogeneity in myocardial structure, created by the altered behaviour of non-myocyte cells, particularly cardiac fibroblasts, which are responsible for collagen synthesis or degradation and thereby fibrous tissue accumulation, is a major determinant for the appearance of diastolic dysfunction and ultimately systolic myocardial failure. Regulatory mechanisms related to this fibrous tissue response are reviewed to draw attention to the hitherto neglected role of cardiac fibroblasts in mediating adverse structural remodelling of the myocardium and showing how this can be prevented through the use of pharmacological agents that interfere with the regulation of the myocardial collagen matrix. Several lines of evidence suggest that circulating and tissue renin-angiotensin-aldosterone systems (RAAS) are involved in the structural remodelling of the non-myocyte compartment. These include the cardioprotective effects of angiotensin converting enzyme (ACE) inhibition and aldosterone receptor antagonism that were found to prevent myocardial fibrosis in the rat with renovascular hypertension. In the rat with genetic hypertension, established left ventricular hypertrophy and abnormal myocardial diastolic stiffness due to interstitial fibrosis, RAAS inhibition resulted in restoration of myocardial structure and function to normal.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Myocardial collagen matrix remodelling in arterial hypertension. 139 56

Ageing of the kidneys has long been associated with a fall in the number of functioning nephrons resulting in a reduction of renal blood flow and glomerular filtration. This narrow concept of age-related changes in renal function has been developed chiefly during the last few years by Brenner et al. on the basis of experimental studies conducted on rodents. According to these authors, the size and frequency of segmental and focal lesions of glomerulosclerosis increase regularly with age, and in its final phase this pathology results in occlusion of glomerular capillaries. Renal ageing, therefore, can be assimilated to the nephron reduction models obtained by surgical ablation. The hypothesis that hypofiltration in certain nephrons is compensated by hyperfiltration in healthy glomerulis, leading to a vicious circle of self-destruction, was then applied to both ageing and experimental renal impairment: the smaller the number of nephrons, the greater the filtration achieved by the remaining nephrons, a process that accelerates the probability of their destruction. Conversely, any attempt to reduce intracapillary pressure or glomerular filtration slows down the progression of renal failure. This hypothesis is supported by experiments showing that reduction of protein intake or chronic inhibition of angiotensin I-converting enzyme activity are truly capable of limiting the progression of glomerulosclerosis induced in rats by partial renal mass ablation. Similarly, prolonged food restriction increases the life expectancy of rodents and almost totally prevents the occurrence of glomerulosclerosis. The experimental finding that degenerative renal lesions do not necessarily develop with age raises the problem of normal and pathological ageing. With an adequate choice of rats' food, strain and sanitary surroundings it is possible to obtain very old animals devoid of occluded glomerular capillaries and loss of nephron. What about the functional and structural changes due to ageing and not to pathology? This question has given rise to numerous studies which concluded, on the whole, that there exists a normal ageing of the kidneys without loss of nephron and that ageing is expressed by the fact that the kidneys have difficulties in adjusting themselves to disturbances in the inner environment. As regards renal functional reserve, response to the antidiuretic hormone in case of water restriction, or stimulation of the renin-angiotensin system in response to decrease of sodium intake, it is clear that the renal cells responsible for glomerular filtration, tubular transport or synthesis and release of peptidic hormones exhibit functional alterations that are age-related. The cellular and molecular mechanisms underlying these physiological changes are little known.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Normal and pathological renal aging in animals]. 140 79

We investigated the role of atrial natriuretic factor (ANF) and the renin-angiotensin system as well as the effects of losartan in rats with aortocaval (AC) shunts. Right atrial and left ventricular end-diastolic pressures (LVEDP) were higher and mean arterial blood pressure (MAP) was lower in AC shunt animals than in their controls. AC shunt rats presented marked cardiac hypertrophy, decreased right atrial ANF concentration, and increased ventricular ANF content and concentration. Plasma ANF levels were elevated, and hematocrit was lower in AC shunt animals than in controls. Captopril or losartan treatment decreased MAP and returned LVEDP to sham-operated control values. A clear regression of cardiac hypertrophy was evident in both treated AC shunt groups, with plasma ANF levels tending to follow those in sham-operated rats. Plasma COOH-terminal ANF levels were decreased and urinary volume and hematocrit were increased in losartan-treated AC shunt animals. We conclude that chronic angiotensin converting enzyme inhibition and angiotension II receptor antagonism improved hemodynamic conditions, diminished water retention, reversed cardiac hypertrophy, and restored plasma and tissue ANF to more "normal" levels in rats with moderate high-output heart failure.
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PMID:Chronic captopril and losartan (DuP 753) administration in rats with high-output heart failure. 141 10


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