Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.23.15 (renin)
 35,795 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

Pulmonary hypertension (PH) is one of the evolutive complications in respiratory diseases leading to chronic respiratory insufficiency (CRI). In most cases PH is mild, but acute worsening can happen and especially during exercise, during sleep (particularly during rapid-eye-movement sleep) and during acute respiratory failure. Usually, pulmonary artery pressure finds again the level observed prior to the worsening. Although PH is usually mild, it is of prognostic value in CRI and particularly in patients with chronic obstructive pulmonary disease (CODP): the survival rate is significantly lower in patients with PH compared with those without PH and the higher PAP is the lower the survival rate. In general, long-term changes in PAP in COPD patients are mild. Long-term oxygen therapy can reverse the progression of PH and increase the survival rate. PH can lead with more or less delay to cor pulmonale and right heart failure (RHF). Oedema can be due to RHF but in some cases they can also be explained by the stimulation of the renin-angiotensin system with increasing of the aldosterone level, due to the fall in renal blood flow. These renal hemodynamic changes are related to arterial blood gas changes (hypercapnic acidosis, hypoxemia).
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PMID:[Pulmonary artery hypertension in chronic respiratory diseases]. 185 23

In 75 COPD patients with (group I) or without (group II) cor Pulmonale, we measured plasma renin activity (PRA), angiotensin I and II (ATI and ATII), and aldosterone (Ald) by RIA. We found that the levels of PRA, ATI, ATII, Ald in group I are all higher than those in 25 healthy subjects and in group II (P less than 0.05, P less than 0.001), The PRA, ATI, ATII, Ald also increased in patients with respiratory failure, especially accompanied by hypercapnia, and in patients with hyponatrium. In addition, the strong correlation was found between PaO2, PaCO2 and RAAS activation. These findings suggest that the activation of RAAS increased significantly in COPD patients with cor pulmonale or with respiratory failure, and the changes may involve in the pathophysiologic process in COPD patients.
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PMID:[The renin-angiotensin-aldosterone system changes in chronic obstructive pulmonary disease]. 263 30

The hemodynamic changes and plasma renin activity (PRA), angiotensin II (ATII), aldosterone (Ald) levels in 38 COPD patients with or without pulmonary hypertension were studied. We found that the right ventricular pressure (RVP), pulmonary artery pressure (PAP), pulmonary vascular resistance (PVR) and the levels of PRA, ATII, Ald increased significantly in patients with pulmonary hypertension when compared with those not accompanied by pulmonary hypertension. In addition, a close correlation was found between PRA, ATII, Ald and RVP, PAP, PVR. The relationship between ATII and PAP was very remarkable (r = 0.67, P less than 0.001). These findings suggest that the activation of renin-angiotensin-aldosterone system (RAAS) increases in COPD patients with pulmonary hypertension, and may involve in the development of pulmonary hemodynamic changes.
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PMID:[Hemodynamic changes and their relationship with the renin-angiotensin-aldosterone system in chronic obstructive pulmonary disease]. 267 85

Disturbances in hormonal systems involved in sodium and water homeostasis are common during respiratory insufficiency. To investigate the role of hypercapnia, we designed a study to examine the hormonal response to acute hypercapnia induced at constant cardiac filling pressures and without hypoxemia. Seven sedated patients with COPD receiving mechanical ventilation were studied during five successive periods. Hemodynamics, arterial blood gases, and plasma hormone levels (atrial natriuretic peptide, renin, angiotensin II, aldosterone, vasopressin) were measured three times during 60 min of acute hypercapnia (52 +/- 5 mm Hg) and at control periods, before (36 +/- 4 mm Hg) and after (42 +/- 3 mm Hg) acute hypercapnia. During acute hypercapnia, mean pulmonary arterial pressure and cardiac output were increased without variation of other measured cardiorespiratory data and hormonal levels when compared with control values. After acute hypercapnia, cardiorespiratory variables returned to control values without variations of hormonal levels. Our results show that moderate acute hypercapnia does not significantly influence the hormonal levels when cardiac filling pressures and sympathetic tone remain stable. We suggest that changes in those plasma hormones involved in salt and water homeostasis during acute hypercapnia are secondary to hemodynamic changes induced by acute respiratory failure and not to acute hypercapnia per se.
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PMID:Effect of acute hypercapnia on alpha atrial natriuretic peptide, renin, angiotensin II, aldosterone, and vasopressin plasma levels in patients with COPD. 787 53

Plasma renin activity (PRA) and aldosterone increase with exercise. Acute hypoxia interferes with this hormonal response to exercise, but the effects of chronic or intermittent hypoxia on exercise-induced hormonal changes are not well understood. The hormonal response to exercise was studied in two groups of subjects who were expected to become hypoxic during exercise (high altitude natives at high altitude and patients with moderate to severe chronic obstructive pulmonary disease or COPD), and normal controls. Both the high altitude natives and COPD patients became hypoxic with maximal exercise. The rate of rise of PRA and epinephrine was significantly less in the two study groups than the normal subjects. Changes in aldosterone levels with exercise were similar to PRA but the differences among groups were not significant. Differences between the groups were not seen for changes in atrial natriuretic polypeptide and norepinephrine during exercise. These results support the concept that hypoxia interferes with the renin-aldosterone and adrenal medullary response to exercise.
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PMID:Hormonal response to exercise in high altitude natives and COPD patients. 833 97

We studied atrial natriuretic factor (ANF), plasma renin activity (PRA), and plasma levels of leukotrienes (LTs) B4 and C4 in 23 patients with COPD undergoing right cardiac catheterization for suspected pulmonary hypertension. Hemodynamic measurements together with concomitant ANF levels (both in venous and pulmonary artery blood and right atrial and pulmonary artery plasma levels of LTC4 and LTB4, were determined at rest (T0), after 30 min of breathing oxygen (3 L/min) (T1), and after 30 min recovering and breathing air (T2). Patients with effective exacerbation or definitive evidence of left ventricular disease, hypertension, arrhythmias, or vasodilator or diuretic therapy were excluded. Increased levels of ANF, both in peripheral venous blood (117 +/- 65 pg/ml) and the pulmonary artery (153 +/- 75 pg/ml), were found in patients with COPD, with or without pulmonary hypertension. Levels of LTC4 were also significantly increased (366 +/- 406 pg/ml) when compared with our control values. No correlations among ANF, LTC4 values, functional tests, and hemodynamic measurements were found. Brief increased levels of oxygen did not modify ANF or LTC4 plasma levels, either in patients with or without pulmonary hypertension.
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PMID:Increased plasma levels of atrial natriuretic factor, renin activity, and leukotriene C4 in chronic obstructive pulmonary disease. 839 99

The renin angiotensin system plays an important role in the development of pulmonary artery remodeling and right ventricular hypertrophy in hypoxia-induced pulmonary hypertension as may occur in patients with COPD. Several polymorphisms of genes encoding for components of the renin angiotensin system such as the M235T polymorphism in the angiotensinogen gene, the 287-base-pair insertion (I)/deletion (D) polymorphism at intron 16 of the ACE gene, and the A1166C polymorphism in the angiotensin II type 1 receptor gene have been associated with an increased risk of cardiovascular diseases. With respect to the pulmonary circulation, only limited data exist on possible associations between polymorphisms of these genes and pulmonary hypertension and/or right ventricular hypertrophy. The objective of the present study was to investigate a possible relationship between polymorphisms of the renin angiotensin system and electrocardiographic evidence of right ventricular hypertrophy in patients with COPD. We therefore determined the angiotensinogen (M235T), angiotensin converting enzyme (I/D), and angiotensin II type 1 receptor (A1166C) genotypes in 87 patients with severe COPD and correlated these data with electrocardiographic parameters of right ventricular hypertrophy. Thirty-one patients (36%) of 87 patients with COPD showed electrocardiographic evidence of right ventricular hypertrophy. In the male, but not in the female, subgroup, the angiotensin-converting enzyme DD genotype was negatively associated with electrocardiographic evidence of right ventricular hypertrophy (male: chi2 = 3.8, p = 0.05; female: chi2 = 0.05, p = 0.82). We found no associations between the investigated polymorphisms in the angiotensinogen and angiotensin II type 1 receptor genes and electrocardiographic evidence of right ventricular hypertrophy.
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PMID:The DD genotype of the angiotensin converting enzyme gene is negatively associated with right ventricular hypertrophy in male patients with chronic obstructive pulmonary disease. 1035 20

We present a two-part review of the English-language literature pertaining to drug therapy for systemic high BP in patients with pulmonary diseases. Part I examines the literature pertaining to the use of antihypertensive drugs in patients with systemic hypertension and coexisting pulmonary conditions, especially COPD and asthma. Part II of the series reviews studies assessing the relationship between sleep-disordered breathing (including the role of the sympathetic nervous system) and systemic hypertension, and presents an approach to the management of these patients. It is the aim of both parts of this review to make qualified conclusions and recommendations applying a methodologic critique to assess the current literature. In the first part of this series, we review the demographics of hypertension in patients with COPD. This is followed by an extensive review of the use of specific classes of antihypertensive drug therapies in patients with pulmonary disease. The antihypertensive agents reviewed include diuretics, calcium antagonists, angiotensin-converting enzyme inhibitors, and angiotensin II receptor antagonists, beta-adrenergic blocking agents, and alpha-beta-blockers and other non-beta-blocker classes. Additionally, the renin angiotensin system is briefly reviewed, with a discussion of how angiotensin-converting enzyme inhibitors induce cough, especially in pulmonary and congestive heart failure patients.
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PMID:Treatment of systemic hypertension in patients with pulmonary disease: COPD and asthma. 1455 4

Several clinical and experimental observations suggest that an intact and activated renin-angiotensin system (RAS) may be an important determinant of erythropoiesis in a variety of clinical conditions, including hypertension, chronic renal insufficiency or failure, chronic obstructive pulmonary disease, and congestive heart failure. Accordingly, RAS inactivation may confer susceptibility to the hematocrit-lowering effects of angiotensin-converting enzyme inhibitors or angiotensin receptor blockers. Indeed, a dose-dependent decrease in hematocrit is observed within the first month of such therapy. In the majority of patients with hypertension decreases in hematocrit values after RAS inactivation are small and not clinically important. In extreme conditions, however, such as erythrocytosis after successful renal transplantation, secondary polycythemia of chronically hypoxemic COPD patients, erythrocytosis associated with renovascular hypertension, severe cardiac or renal failure, the hematocrit-lowering effect of angiotensin-converting enzyme inhibitors and angiotensin receptor blocker may be profound and even lead to or worsen anemia. Hematocrit reaches its nadir value within three months, and then it remains stable during long-term observations. After discontinuation of RAS blockade, hematocrit values rise gradually over the next three to four months towards the pretreatment levels. The mechanism(s) related to this phenomenon is not yet fully understood, but angiotensin II seems to be responsible for inappropriately sustaining secretion of erythropoietin despite hematocrit elevation and capable to directly stimulate the erythroid progenitors in bone marrow to produce erythrocytes.
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PMID:Hematocrit-lowering effect following inactivation of renin-angiotensin system with angiotensin converting enzyme inhibitors and angiotensin receptor blockers. 1496 14


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