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)

Aim of the study was to evaluate the effect of cardiopulmonary receptors activation and deactivation on antidiuretic hormone (ADH) and atrial natriuretic peptide (ANP) incretion in hypertensive and normotensive subjects. Twenty-one male subjects, 7 normotensives and 14 mild hypertensives, 7 without and 7 with left ventricular hypertrophy (LVH) were admitted to the study. Each subject underwent selective loading and unloading of cardiopulmonary receptors, by application of a positive (LBPP) or negative (LBNP) pressure to the lower body. Blood samples were taken for measurement of ANP, ADH, PRA, immunoreactive renin, aldosterone, noradrenaline and adrenaline. ADH plasma concentration increased during cardiopulmonary receptors inhibition, but this increase became statistically significant (p less than 0.05) at a step of LBNP (-40 mm Hg), in which an involvement of the sinoaortic receptors cannot be excluded. ANP plasma levels increased progressively during LBPP (p less than 0.05 at least). These changes were significantly reduced in hypertensive patients with LVH.
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PMID:Antidiuretic hormone and atrial natriuretic peptide during lower body negative or positive pressure in hypertensive patients with and without left ventricular hypertrophy. 138 63

A survey of the mechanisms of stimulation of secretion and of atrial natriuretic peptide (ANP) and its action is presented. Action of this hormone is particularly important on the kidney, the cardiovascular system and on some endocrine tissues. Major secretory organs are atrial myocytes, with an increased intra-atrial pressure as the stimulus. Under the action of ANP occurs dilatation of arterial blood vessels, often masked in vivo by a secondary increase in the sympathetic tone. ANP decreases the venous return with consecutive lowering of cardiac output. In a kidney an increase in diuresis and natriuresis occurs. Among the actions on the endocrine tissues inhibition of aldosterone secretion and, most probably, inhibition of renin secretion, are the most important.
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PMID:[Atrial natriuretic peptide. Mechanisms of its action]. 138 77

Endothelin-1, a potent vasoconstrictor peptide with 21 amino acid residues, is released by the vascular endothelium. Plasma immunoreactive endothelin levels were measured in 23 patients with cirrhosis and in 20 healthy subjects. Concentrations were significantly lower in patients with non-uraemic cirrhosis than in normal subjects (19.4 +/- 8.9 pmol/l vs. 48.8 +/- 24.8 pmol/l, p less than 0.002). Plasma renin, aldosterone, atrial natriuretic peptide, arginine-vasopressin and catecholamines did not show significant correlations with plasma endothelin-1 levels. Furthermore, there were no significant differences in plasma endothelin levels for etiology of cirrhosis, presence of ascites or varices. These data suggest that low circulating endothelin may be involved in the development or maintenance of systemic vasodilatation in cirrhosis.
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PMID:Plasma endothelin levels in cirrhotic subjects. 138 39

Sodium excretion and the blood levels of aldosterone, renin, atrial natriuretic peptide (ANP), and insulin were investigated in 9 women with obesity of alimentary-constitutional type during hunger therapy and resumed nutrition. It has been assumed that restricted sodium excretion with the kidneys during fasting is mainly caused by activation of the renin-angiotensin-aldosterone system, with ANP contributing to it, insulin not playing the major role in this process.
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PMID:[Hormonal regulation of sodium excretion by the kidneys during hunger therapy of obese patients]. 138 80

1. Two hours after a single dose of indomethacin (INDO), plasma renin activity (PRA) and atrial natriuretic peptide (ANP) levels decreased, which is consistent with an effect of lowering prostaglandins (PG). 2. After 48 h of INDO, PRA remained low but ANP had increased, which is consistent with the known effect of prostaglandin inhibitors to cause sodium retention, with a resulting volume expansion. 3. Infusions of angiotension II (AII), which raises diastolic blood pressure (BP) 20 mmHg or more, consistently raised ANP levels. The ANP response to AII infusion was reduced 48 h after INDO, which is consistent with an important role for PG in AII-stimulated ANP release. 4. After PG were blocked with INDO, the stimulating effect of AII on ANP at doses that increased diastolic BP less than 20 mmHg was insignificant, whereas before INDO it was significant. 5. In dose-response studies, INDO increased the systolic BP response but decreased the ANP response to AII, which is consistent with a direct effect of PG on ANP that is independent of systolic BP. 6. Prostaglandins and BP are important in the ANP response to AII infusion in normal subjects, but AII itself appears to have little direct effect on ANP.
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PMID:Prostaglandins and systolic blood pressure, but not angiotensin II, independently affect atrial natriuretic peptide levels in man. 138 41

Increasing evidence indicates that angiotensin II can be formed by juxtaglomerular cells (JGC) and cosecreted with renin. We investigated the existence of this local renin-angiotensin system in a human JGC tumor, using an in vitro superfusion. The JGC tumor was found concomitantly to release renin and angiotensin I and II. Sequential addition of atrial natriuretic peptide, dopamine, and a somatostatin analog in the superfusion did not affect renin or angiotensin I and II release. The data provide evidence that the human JGC tumor in vitro generates angiotensin II, and supports its possible role as a local in vivo regulator of kidney function.
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PMID:Concomitant release of renin, angiotensin I, and angiotensin II during superfusion of human juxtaglomerular cell tumor. 138 67

The association of liver cirrhosis with arterial essential hypertension has been previously described. The present study extends the previous reports by investigating the hormonal relationships that may occur in patients with established essential hypertension associated to liver cirrhosis. We studied the renin-angiotensin, the adrenergic systems and other vasoactive hormones such as arginine-vasopressin, atrial natriuretic peptide, endothelin and parathyroid hormone in cirrhotic patients with and without essential hypertension. The data suggested that the coincidence of arterial hypertension in cirrhotic patients was characterized by the following findings: a decreased renin-angiotensin activity; a reduced systemic vasodilatation; an increased peripheral pressor effect of vasoactive hormones and an increased effective blood volume.
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PMID:Hormonal aspects of the relation of liver cirrhosis to essential hypertension. 139 76

1. The control of extracellular fluid volume (ECFV) in normal pregnancy may be related to changes in atrial natriuretic peptide. Previous studies in non-pregnant subjects have suggested that plasma atrial natriuretic peptide (ANP) increases in response to dietary sodium supplementation because of an increase in plasma volume, although this has not been measured directly. 2. Nine women who were pregnant in the third trimester undertook oral sodium supplementation (136 mmol) for 5 days in addition to their usual diet. Twenty-four hour urinary sodium excretion increased by 125 +/- 54 mmol/day (mean +/- s.d.; P less than 0.01). Plasma volume was unchanged, although total ECFV tended to increase (P less than 0.09 and bodyweight increased (1.3 +/- 1.4 kg; P less than 0.01) at the end of these diets. 3. Plasma ANP increased by 30.7 [8.6, 34.5] pmol/L (median [25th, 75th percentile]; P less than 0.05), while plasma renin concentration decreased significantly from 7.3 [6.2, 11.2] to 2.6 [1.7, 3.9] pmol angiotensin I/mL (P less than 0.01), as did plasma aldosterone concentration (1435 [1162, 1722] to 753 [595, 1110] fmol/mL; P less than 0.01). Plasma vasoactive intestinal peptide was unchanged. 4. Pregnant women respond to increased dietary sodium with an increase in plasma ANP in the absence of a significant increase in plasma volume. The acute regulation of plasma ANP in response to increases in dietary sodium in pregnant women does not appear to be mediated by changes in intravascular fluid volume.
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PMID:Atrial natriuretic peptide in pregnancy: response to oral sodium supplementation. 139 5

Congestive heart failure is the most common cause of death in young adults with thalassaemia major. In the present study we compared atrial natriuretic peptide levels (ANP) in 30 asymptomatic patients with thalassaemia major (aged 16.6 +/- 6.4 years), normal left ventricular diastolic cavity dimension and systolic function, with 30 aged and sex matched normal control subjects. ANP levels were significantly higher in patients with thalassaemia major compared to controls (93.9 +/- 26.3 pg.ml-1 vs 51.8 +/- 26.5 pg.ml-1; P < 0.001). Plasmatic renin activity, aldosterone, urinary sodium and catecholamine levels at basal conditions did not differ significantly in these two groups (ns). Blood volume stimulation (blood transfusion) in thalassaemic patients was followed by an increase of mean ANP values (93.9 +/- 26.3 to 109.1 +/- 40.5 pg.ml-1; P < 0.03). ANP basal levels above two standard deviations of the mean values obtained in normal control subjects were considered as abnormal and found to be in close correlation with the presence of diastolic dysfunction of the left ventricle identified by Doppler echocardiography. The method has a 57% sensitivity and a 91% specificity for revealing pre-clinical cardiac involvement (P < 0.02). Although a longer observation period is necessary in order to define the clinical and prognostic significance of these data, our results show that an increase in ANP basal values is present in asymptomatic patients with thalassaemia major. This suggests initial myocardial involvement, while ANP response to volume overload is maintained.
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PMID:Cardiac involvement in thalassaemia major: altered atrial natriuretic peptide levels in asymptomatic patients. 139 10

The levels of several regulatory peptides were measured in peripheral plasma samples from individuals with chronic cardiac failure (CCF) and matched controls in both the resting state and during a short period of maximal exercise. Basal levels of noradrenaline (NA; 705 +/- 114 vs 195 +/- 54 ng.l-1; mean +/- SEM; P < 0.05), plasma renin activity (PRA; 12.9 +/- 2.9 vs 2.1 +/- 0.3 ng AI ml-1.h-1; P < 0.05) and aldosterone (ALDO; 325 +/- 49 vs 87 +/- 8 ng.l-1; P < 0.05) were all raised in the patients with CCF, and increased further with exercise. Basal circulating levels of atrial natriuretic peptide (ANP) were also significantly higher in the CCF group compared to controls (136 +/- 35 vs 27 +/- 5 ng.l-1; P < 0.01), but the response to exercise was attenuated, so that at peak exercise, no significant difference was observed. Basal circulating levels of gastrin-releasing peptide (GRP) (29 +/- 4 vs 40 +/- 4 ng.l-1; P < 0.05) and secretin (13 +/- 1 vs 32 +/- 4 ng.l-1; P < 0.05) were significantly lower in the CCF group when compared to controls and there was no significant change in the levels of either peptide with exercise. Levels of neurokinin A (NKA), neuropeptide Y (NPY) and neurotensin (NT) were somewhat higher in patients, but the differences were not significant, and there were no changes during exercise. There were also no significant differences in the levels of vasoactive intestinal peptide (VIP), glucose-dependent insulinotropic polypeptide (GIP), insulin or glucagon in either experimental group both before and during exercise. We have therefore identified different circulating levels of certain regulatory peptides in patients with CCF, but the significance of these remains unclear.
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PMID:Regulatory peptides in the plasma of patients with chronic cardiac failure at rest and during exercise. 139 15


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