The significance of body sodium content in hypertension following renal transplantation: Exchangeable sodium and plasma renin concentration before and after renal transplantation

1977 ◽  
Vol 37 (4) ◽  
pp. 295-301 ◽  
Author(s):  
H. J. Kornerup
Keyword(s):  
Renal Transplantation ◽  
Plasma Renin ◽  
Sodium Content ◽  
Exchangeable Sodium ◽  
Plasma Renin Concentration ◽  
Body Sodium ◽  
Before And After

SERIAL ESTIMATION OF PLASMA RENIN CONCENTRATION DURING PREGNANCY AND AFTER PARTURITION

1966 ◽  
Vol 35 (4) ◽  
pp. 373-378 ◽  
Author(s):  
J. J. BROWN ◽  
D. L. DAVIES ◽  
P. B. DOAK ◽  
A. F. LEVER ◽  
J. I. S. ROBERTSON
Keyword(s):  
Pregnant Women ◽  
Plasma Renin ◽  
Plasma Renin Concentration ◽  
Before And After ◽  
Normal Women ◽  
Made In

SUMMARY Plasma renin concentration has been measured in normal women at intervals throughout pregnancy. Further measurements have been made in the days and hours before and after delivery of the foetus and placenta. Plasma renin was consistently raised in the majority of pregnant women and did not change markedly until 24 hr. or more after delivery. The significance of these findings is discussed.

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.

Role of the Kidney in ‘Salt and Water Dependent Hypertension’ of End-Stage Renal Disease

1972 ◽  
Vol 42 (1) ◽  
pp. 47-55 ◽  
Author(s):  
G. Bianchi ◽  
C. Ponticelli ◽  
U. Bardi ◽  
B. Redaelli ◽  
L. Campolo ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Renal Disease ◽  
End Stage Renal Disease ◽  
Salt Intake ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Plasma Renin Concentration ◽  
Body Sodium ◽  
Stage Renal Disease ◽  
End Stage

1. Blood pressure, plasma renin concentration, exchangeable body sodium, plasma volume and extracellular fluid volume were measured in five patients on maintenance haemodialysis for end-stage renal disease in whom hypertension was relatively easy to control by the combination of dialysis and restriction of salt intake. Measurements were made on three occasions: on a free salt intake the day before dialysis; on a low salt intake the day after dialysis; on a free salt intake the day before dialysis after nephrectomy. 2. The fall of blood pressure after haemodialysis and salt intake restriction was accompanied by a decrease of exchangeable body sodium and body fluids while plasma renin concentration increased. The fall of blood pressure after bilateral nephrectomy was accompanied by a fourfold decrease of plasma renin without any change of the other variables. 3. The hypertension of these patients might thus be considered ‘salt and water dependent’ or ‘renin dependent’ according to the means used to decrease blood pressure.

Exchangeable Sodium in Experimental Hypertension in Rats

1976 ◽  
Vol 51 (s3) ◽  
pp. 133s-135s
Author(s):  
A. E. Doyle ◽  
S. Duffy ◽  
G. J. MacDonald
Keyword(s):  
Blood Pressure ◽  
Renal Artery ◽  
Severe Hypertension ◽  
Plasma Renin ◽  
The Other ◽  
Left Renal Artery ◽  
Experimental Hypertension ◽  
Exchangeable Sodium ◽  
Before And After

1. Total exchangeable sodium was measured in rats by a radio-sodium equilibration method, before and after the production of hypertension by clipping the left renal artery, with or without contralateral nephrectomy. 2. Clipping of one renal artery with removal of the other kidney produced severe hypertension with no significant changes in exchangeable sodium or plasma renin levels. 3. Clipping of one renal artery without contralateral nephrectomy produced severe hypertension in some animals, but little change in blood pressure in others. The animals which developed severe hypertension had a marked increase in exchangeable sodium with a concomitant rise in plasma renin; the animals with smaller rises in blood pressure did not have these changes. 4. The fact that both plasma renin levels and exchangeable sodium levels increase according to this method, suggests that hypertension in the two-kidney model is renin-dependent.

Effect of Haemorrhage on Renin Concentration in Superficial and Deep Venous Outflows of the Cat Kidney

1981 ◽  
Vol 60 (6) ◽  
pp. 703-706 ◽  
Author(s):  
Susan M. Jones ◽  
J. Torretti
Keyword(s):  
Blood Pressure ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Venous Drainage ◽  
Renin Release ◽  
Venous Outflow ◽  
Plasma Renin Concentration ◽  
Before And After ◽  
Arterial Plasma ◽  
Cortical Venous Drainage

1. Plasma renin concentration is significantly higher in the subcapsular venous outflow, which drains the superficial cortex, than in the deep venous outflow, which drains the inner half of the cortex and medulla of the cat kidney. The purpose of these experiments was to observe whether this pattern is preserved or disrupted by a stimulus to renin release. 2. Plasma renin concentration in arterial samples and in the superficial and deep renal venous outflows was measured before and after haemorrhage which produced a 24 ± 6.7% drop in mean blood pressure in 13 cats. 3. After haemorrhage, total kidney plasma flow and glomerular filtration rate (GFR) did not change significantly. There was a rise in arterial plasma renin concentration. Venous minus arterial plasma renin concentration increased significantly in the deep venous outflow, but not in the superficial outflow. 4. The results suggest that both superficial and deep cortical venous drainage of the cat kidney should be considered when measuring renal renin release. In addition, they suggest that there may be differences in the response of superficial and deep juxtaglomerular apparatuses to haemorrhage.

The Estimation of Plasma Renin Concentration in the Dog

1964 ◽  
Vol 93 (1) ◽  
pp. 3C-4C ◽  
Author(s):  
J. J. Brown ◽  
D. L. Davies ◽  
A. F. Lever ◽  
J. I. S. Robertson ◽  
M. Tree
Keyword(s):  
Plasma Renin ◽  
Plasma Renin Concentration

EXTRAHEPATIC AND EXTRARENAL RENIN INACTIVATION IN THE DOG

1974 ◽  
Vol 60 (2) ◽  
pp. 217-222
Author(s):  
R. FAGARD ◽  
E. FOSSION ◽  
M. CAMPFORTS ◽  
A. AMERY
Keyword(s):  
Blood Vessels ◽  
Pulmonary Circulation ◽  
Plasma Renin ◽  
Glass Container ◽  
Plasma Renin Concentration ◽  
Vascular Beds ◽  
Extrarenal Renin

SUMMARY It was demonstrated previously that renin disappears quickly from the circulation after nephrectomy in the hepatectomized dog. In the present study the plasma renin concentration (PRC) was measured in the efferent and afferent blood vessels of several vascular beds (pulmonary circulation, splanchnic region, spleen, both inferior limbs and pelvis, head) in the anhepatic and in the anhepatic and anephric dog in order to investigate extrarenal and extrahepatic renin inactivation. However, no significant arteriovenous differences in PRC could be traced. The blood of these dogs kept in vitro at 37 °C in a glass container showed no decline in PRC within 3 h of removal. Therefore no specific extrahepatic and extrarenal renin-inactivating mechanism was found which could explain the rapid disappearance of renin from the blood in vivo in the anhepatic and anephric dog.

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