Evidence for the Renal Origin of the Natriuretic Hormone

2015 ◽  
pp. 165-181 ◽  
Author(s):  
I. H. Mills
Keyword(s):  
Natriuretic Hormone ◽  
Renal Origin

The Kidney and Fibrinolysis

1970 ◽  
Vol 24 (01/02) ◽  
pp. 026-032 ◽  
Author(s):  
N. A Marsh
Keyword(s):  
Molecular Weight ◽  
Plasminogen Activator ◽  
Enzyme System ◽  
Normal Animal ◽  
Fibrinolytic Enzyme ◽  
The Other ◽  
Exclusion Chromatography ◽  
Normal Urine ◽  
Renal Origin ◽  
Molecular Exclusion Chromatography

SummaryMolecular exclusion chromatography was performed on samples of urine from normal and aminonucleoside nephrotic rats. Normal urine contained 2 peaks of urokinase activity, one having a molecular weight of 22,000 and the other around 200,000. Nephrotic urine contained three peaks of activity with MW’s 126,000, 60,000 and 30,000. Plasma activator determined from euglobulin precipitate had a MW. in excess of 200,000. The results indicate that in the normal animal, plasma plasminogen activator does not escape into the urine in substantial quantities but under the conditions of extreme proteinuria there may be some loss through the kidney. The alteration in urokinase output in nephrotic animals indicates a greatly disordered renal fibrinolytic enzyme system.The findings of this study largely support the hypothesis that plasma plasminogen activator of renal origin and urinary plasminogen activator (urokinase) are different molecular species.

Overview of Treatment Options for Critical Limb Ischaemia Patients

2011 ◽  
Vol 7 (1) ◽  
pp. 51 ◽  
Author(s):  
Frederic Baumann ◽  
Nicolas Diehm ◽  
◽  
Keyword(s):  
Treatment Options ◽  
Critical Limb Ischaemia ◽  
Treatment Modalities ◽  
High Morbidity ◽  
Limb Ischaemia ◽  
Arterial Revascularisation ◽  
Planning Treatment ◽  
Treatment Concepts ◽  
Peripheral Arterial ◽  
Renal Origin

Patients with critical limb ischaemia (CLI) constitute a subgroup of patients with particularly severe peripheral arterial occlusive disease (PAD). Treatment modalities for these patients that often exhibit multilevel lesions and severe vascular calcifications are complicated due to multiple comorbidities, i.e. of cardiac and vascular but also of renal origin. These need to be taken into consideration while planning treatment options. Although CLI is associated with considerably high morbidity and mortality rates, the clinical outcome of patients being subjected to revascularisation has improved substantially in recent years. This is mainly due to improved secondary prevention strategies as well as dedicated endovascular innovations for this most challenging patient cohort. The aim of this article is to provide a discussion of the contemporary treatment concepts for CLI patients with a focus on arterial revascularisation.

NATRIURETIC PEPTIDES LEVEL AND THE STATUS OF THE RENIN – ANGIOTENSIN-ALDOSTERONE SYSTEM IN CHRONIC KIDNEY DISEASE IN PATIENTS WITH CONGENITAL MALFORMATIONS OF THE URINARY SYSTEM

2018 ◽  
Vol 22 (5) ◽  
pp. 45-50
Author(s):  
A. M. Mambetova ◽  
A. M. Inarokova ◽  
N. N. Shabalova ◽  
D. V. Bizheva ◽  
A. T. Mahiyeva
Keyword(s):  
Congenital Malformations ◽  
Control Group ◽  
Healthy Children ◽  
Urinary System ◽  
Renin Angiotensin Aldosterone System ◽  
Natriuretic Hormone ◽  
Renin Angiotensin ◽  
Group I ◽  
The Status ◽  
Sick Children

THE AIM. To determine the concentration of natriuretic peptide in the blood serum in children with congenital malformations of the urinary system (CM US) and to compare with the activity of renin-angiotensin-aldosterone system (RAAS).MATERIALS AND METHODS.119 patients with CM US aged 3 to 18 years were examined. A control group of 10 clinically healthy children. 3 groups were assigned: group I – 55 children with  congenital vesicoureteral reflux, and group II – 34 children with  congenital hydronephrosis and ureterohydronephrosis, III group – 30 children with other forms of dysembryogenesis of the US. Following indicators were identified by ELISA in the blood: renin, aldosterone,  N – terminal propeptide natriuretic hormone (NT-рroВNР). RESULTS.NT-рroВNР, renin and aldosterone hyperproduction were diagnosed in 59,6%, 69,7%, 54.6 % of sick children relatively. Concentrations were higher in all variants of  malformations in comparison with the control group. Significant  differences were revealed in obstructive species, where arterial  hypertension (AH) was diagnosed more often. Patients with AH  recorded significantly higher concentrations of NT-proВNР and renin.CONCLUSION.The key point in pathological processes developmentand progression in the cardiovascular system and kidneys is the  activation of RAAS. The system of natriuretic factors is important in maintaining the compensated state of patients due to the blockade of RAAS.

A novel biological effect of atrial natriuretic hormone: Inhibition of mesangial cell mitogenesis

1988 ◽  
Vol 152 (2) ◽  
pp. 893-897 ◽  
Author(s):  
Adam Johnson ◽  
Ferzan Lermioglu ◽  
Uttam C. Garg ◽  
Rebecca Morgan-Boyd ◽  
Aviv Hassid
Keyword(s):  
Biological Effect ◽  
Mesangial Cell ◽  
Natriuretic Hormone ◽  
Atrial Natriuretic Hormone ◽  
Atrial Natriuretic

Elevation of sodium levels in the cerebral ventricles of anaesthetized dogs triggers the release of an inhibitor of ouabain-sensitive sodium, potassium-ATPase into the circulation

1986 ◽  
Vol 70 (1) ◽  
pp. 103-110 ◽  
Author(s):  
Bhagavan S. Jandhyala ◽  
Ahmad F. Ansari
Keyword(s):  
Blood Vessels ◽  
Circumventricular Organs ◽  
Plasma Samples ◽  
Cerebral Ventricles ◽  
Sodium Potassium ◽  
Natriuretic Hormone ◽  
Circulating Blood Volume ◽  
Na Pump ◽  
Artificial Cerebrospinal Fluid ◽  
Uptake Method

1. The present studies are designed to determine whether a ouabain-sensitive inhibitor of Na+, K+−stimulated ATPase is released into the circulation when the Na+ levels are elevated in the cerebral ventricles in pentobarbital anaesthetized dogs. Na+−pump activity was estimated in the plantar and dorsal branches of the lateral saphenous veins by using the 86Rb-uptake method. 2. Infusion of the cerebral ventricles with the artificial cerebrospinal fluid (CSF) containing normal Na+ (0.15 mol/l) for over 120 min resulted in significant increases in only ouabain-sensitive 86Rb-uptake. In contrast, when the ventricles were perfused with the CSF containing high Na+ (0.3 mol/l) for similar periods, there were significant reductions in the ouabain-sensitive as well as in ouabain-insensitive 86Rb-uptake by the blood vessels. 3. Similar blood vessels from a separate group of dogs were incubated for 120 min in the plasma samples collected from the above groups in which normal or hypertonic Na+ solutions were infused. The data showed that ouabain-sensitive 86Rb-uptake (but not the insensitive component) was significantly inhibited only in those vessels which were incubated in the plasma samples that were obtained at 120 min after perfusion of the cerebral ventricles with CSF containing high Na+ (0.3 mol/l). 4. These studies have provided direct evidence which would suggest that the elevation of Na+ levels in the cerebral ventricles would precipitate the release of an inhibitor of the ouabain-sensitive Na+−pump into the circulation, perhaps due to an activation of Na+−sensitive and/or osmo-sensitive sites in the circumventricular organs. It is hypothesized that this humoral substance may be the same ‘natriuretic hormone’ which is released after acute expansion of circulating blood volume.

CONGENITAL PITRESSIN RESISTANT DIABETES INSIPIDUS OF RENAL ORIGIN

PEDIATRICS ◽  
1955 ◽  
Vol 15 (3) ◽  
pp. 298-372
Author(s):  
William B. Macdonald
Keyword(s):  
Diabetes Insipidus ◽  
Extracellular Fluid ◽  
Male Infant ◽  
Renal Tubules ◽  
Post Mortem ◽  
Water Metabolism ◽  
History Of ◽  
Renal Clearances ◽  
Renal Function Tests ◽  
Renal Origin

1) The history of a male infant who presented soon after birth with features of failure to gain weight, dehydration and pyrexia of obscure origin, has been described. A diagnosis of pitressin resistant diabetes insipidus was made. 2) Renal function tests and post-mortem examination, including microdissection of the kidney, indicates that the basic defect in water metabolism was a functional inability of the distal renal tubules to respond to antidiuretic hormone. 3) Consequent dehydration was insufficient to cause circulatory collapse, but affected renal clearances. 4) There was evidence of increased catabolism and poor protein utilisation. 5) Hyperosmolarity of the extracellular fluid was accompanied by a rise in body temperature, probably due to a depression of sweat gland activity. 6) Post-mortem evidence suggests that infants with pitressin resistant diabetes insipidus should be investigated for cystine storage disease.

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