Active and inactive renin in dog plasma before and after bilateral nephrectomy

1981 ◽  
Vol 37 (7) ◽  
pp. 785-786 ◽  
Author(s):  
J. Staessen ◽  
P. Lijnen ◽  
R. Fagard ◽  
A. Amery
Keyword(s):  
Bilateral Nephrectomy ◽  
Dog Plasma ◽  
Before And After ◽  
Inactive Renin

Active renin and renin glycoform dynamics in the carotid artery

1996 ◽  
Vol 271 (1) ◽  
pp. H184-H191
Author(s):  
S. A. Katz ◽  
J. A. Opsahl ◽  
L. M. Forbis ◽  
W. Ayenew
Keyword(s):  
Carotid Artery ◽  
Aortic Wall ◽  
Plasma Renin ◽  
Vascular Wall ◽  
Bilateral Nephrectomy ◽  
Plasma Renin Concentration ◽  
Active Renin ◽  
Before And After ◽  
Carotid Wall ◽  
Renal Origin

Active renin and five major active renin glycoforms were measured in plasma and the carotid wall of anesthetized rabbits before and after 1.5- and 24-h bilateral nephrectomy (BNX). Before BNX, there was no difference in renin glycoform proportions between plasma and the carotid wall. Plasma renin concentration (PRC) fell by 67% after 1.5-h BNX due to preferential clearance of renin glycoforms I+II, but no significant change in renin concentration was seen in the carotid artery (or aorta). Twenty-four hours after BNX, PRC and carotid wall renin concentrations were reduced by 99.7 and 97.7%, respectively, while the proportion of renin glycoforms I+II in the carotid wall was significantly elevated. These data are consistent with the view that vascular renin is derived from plasma renin of renal origin. After BNX, renin disappearance from the carotid (and aortic wall) is slower than renin decay from plasma, and the less negatively charged active renin glycoforms I+II exit the carotid wall much more slowly than the more negatively charged glycoforms. After 24-h BNX, renin glycoforms I+II were still effluxing from the vascular wall and represented the only glycoforms present in the carotid wall.

Active and Inactive Renin in Individual Juxtaglomerular Apparatuses

1980 ◽  
Vol 59 (s6) ◽  
pp. 35s-36s
Author(s):  
A. Gillies ◽  
T. Morgan ◽  
W. Fitzgibbon
Keyword(s):  
Salt Intake ◽  
Active Form ◽  
Juxtaglomerular Apparatus ◽  
Macula Densa ◽  
Active Renin ◽  
High Salt Intake ◽  
Before And After ◽  
Inactive Renin ◽  
Inhibitor Of Protein Synthesis

1. Renin was measured in individual juxtaglomerular apparatuses before and after acidification in vitro.. 2. Active renin increased with delivery of extra sodium by microperfusion to the macula densa and this increase was similar to that achieved with acidification. 3. In rats pretreated with an inhibitor of protein synthesis active renin increased when extra sodium was delivered to the macula densa. 4. Salt intake changed the amount of renin present in the juxtaglomerular apparatus. In rats on a high salt intake the total renin was low and was all in an active form.

scholarly journals The Role of the Kidney in the Production of the Erythropoietic Factor

Blood ◽  
1960 ◽  
Vol 16 (6) ◽  
pp. 1770-1776 ◽  
Author(s):  
JEAN-PIERRE NAETS
Keyword(s):  
Red Cells ◽  
Bilateral Nephrectomy ◽  
Erythropoietic Activity ◽  
Dog Plasma

Abstract The role of the kidney in production of erythropoietin was investigated. Dogs were made anemic by phlebotomy and were then subjected to bilateral nephrectomy, ureter ligation or ureter section. Erythropoietic stimulating activity in the dog plasma was judged by measuring the incorporation of Fe59 into the red cells of starved rats. No erythropoietic activity could be found in the dog plasma 24 and 48 hours after nephrectomy, but erythropoietic activity was found after ligation of the ureters.

Quantitation of Inactive Renin in Human and Dog Plasma: Techniques for Activation

1982 ◽  
Vol 4 (11-12) ◽  
pp. 2185-2191 ◽  
Author(s):  
J. E. Sealey ◽  
J. F. Gallagher ◽  
S. A. Atlas ◽  
T. E. Hesson ◽  
J. H. Laragh
Keyword(s):  
Dog Plasma ◽  
Inactive Renin ◽  
Plasma Techniques

Inactive Renin in Rabbit Plasma: Effect of Haemorrhage

1979 ◽  
Vol 56 (2) ◽  
pp. 105-108 ◽  
Author(s):  
H. K. Richards ◽  
S. A. Grace ◽  
A. R. Noble ◽  
K. A. Munday
Keyword(s):  
Blood Vessels ◽  
Renin Activity ◽  
Bilateral Nephrectomy ◽  
Rabbit Plasma ◽  
Inactive Form ◽  
Inactive Renin ◽  
Plasma Effect

1. Renin activity in rabbit plasma increases after acidification (pH 3·3), probably due to activation of an inactive form of renin. 2. Both active and inactive renin in plasma increase after haemorrhage. This stimulus does not change the relative proportions of the two forms. 3. After ligation of the renal blood vessels neither form of renin increases in response to haemorrhage. 4. One day after bilateral nephrectomy no inactive renin could be demonstrated in plasma. 5. In the rabbit, therefore, the kidney is a major source of the inactive renin in plasma.

The initial uptake of copper by the liver in the dog

1968 ◽  
Vol 46 (5) ◽  
pp. 771-784 ◽  
Author(s):  
Carl A. Goresky ◽  
Thomas H. Holmes ◽  
Andrew Sass-Kortsak
Keyword(s):  
Plasma Concentrations ◽  
Hepatic Uptake ◽  
Constant Infusion ◽  
Multiple Indicator Dilution ◽  
Dog Plasma ◽  
Major Organ ◽  
Before And After ◽  
Multiple Indicator ◽  
Wet Weight ◽  
Initial Uptake

The initial uptake of 64Cu and serum and tissue copper levels were examined in the dog. Plasma disappearance curves, multiple indicator dilution studies of initial hepatic uptake, and constant infusion experiments were carried out, at various doses, before and after preloading with cupric acetate. Over a range of plasma concentrations of direct-reacting copper extending to levels far above those encountered under physiological circumstances, little evidence of saturation of the initial hepatic uptake was evident. The countertransport of labeled copper was produced by administering unlabeled copper. The tissue levels of copper in the liver of the normal dog were, unexpectedly, found to be comparatively high, to average 82 μg/g wet weight. Attempts to produce manyfold increases in this copper content by daily intravenous copper administration failed because the doses of copper which would have been necessary to produce the increases, doses which would not have caused major toxic effects in the rat, were lethal for the dog. This low tolerance for copper loading presumably reflects the preexisting high copper concentration in the liver, the major organ which takes up exogenously administered copper. The degree of preloading which could be achieved produced no perceptible change in initial hepatic uptake. The copper levels in the liver are of the order of those found in some patients with Wilson's disease. Despite this, none of the other abnormalities which characterize this disease have been encountered in dogs.

The Role of Sodium Retention in Goldblatt 2-Kidney Hypertension in the Rat

1976 ◽  
Vol 51 (s3) ◽  
pp. 125s-127s
Author(s):  
H. Thurston ◽  
J. D. Swales
Keyword(s):  
Blood Pressure ◽  
Renin Angiotensin System ◽  
Sodium Retention ◽  
Bilateral Nephrectomy ◽  
Hypertensive Rats ◽  
Short Term ◽  
Angiotensin System ◽  
Angiotensin Ii Antagonist ◽  
Before And After

1. Infusion of angiotensin II antagonist failed to restore the blood pressure of short-term Goldblatt 2-kidney hypertensive rats to normal levels before and after sodium restriction. 2. The blood pressure of both normal and sodium-restricted Goldblatt 2-hypertensive rats remained elevated 6 h after bilateral nephrectomy. 3. The residual hypertension found during antagonist infusion and after bilateral nephrectomy is not maintained by the renin—angiotensin system or sodium retention.

Fibrinolytic Activators and Inhibitors in Terminal Renal Insufficiency and in Anephric Patients

1984 ◽  
Vol 52 (03) ◽  
pp. 311-314 ◽  
Author(s):  
E J P Brommer ◽  
I Schicht ◽  
G Wijngaards ◽  
J H Verheijen ◽  
D C Rijken
Keyword(s):  
Renal Insufficiency ◽  
Fibrinolytic Activity ◽  
Baseline Level ◽  
Healthy Controls ◽  
Bilateral Nephrectomy ◽  
Α2 Macroglobulin ◽  
Before And After ◽  
Normal Increase ◽  
Anephric Patients

SummaryFibrinolytic factors were measured before and after DDAVP- infusion in 18 patients on chronic, regular haemodialysis, 11 of whom underwent bilateral nephrectomy, and in 7 patients in whom non-functioning kidneys were still present. Baseline fibrinolytic activity was normal or high in all but two cases. Before haemodialysis, the response to DDAVP-infusion was greatly reduced in the majority of patients as compared with healthy controls, irrespective of the baseline level. This was in accordance with mean t-PA-antigen levels which increased only slightly after DDAVP. When DDAVP was given after haemodialysis, previous non-responders showed a normal increase in fibrinolytic activity. The level of free t-PA-inhibitors was normal in most cases as were levels of α2-antiplasmin. and α2-macroglobulin.

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