The Clearance of Endogenous Renin in the Anhepatic Anephric Dog

1973 ◽  
Vol 45 (s1) ◽  
pp. 225s-228s
Author(s):  
R. Fagard ◽  
E. Eyskens ◽  
H. Delooz ◽  
E. Fossion ◽  
A. Amery
Keyword(s):  
Plasma Renin ◽  
Plasma Renin Concentration ◽  
Rapid Fall ◽  
Inferior Limb

1. A rapid fall in plasma renin concentration occurs not only in colonectomized but also in hepatectomized dogs after binephrectomy. 2. In the anhepatic anephric dog no renin extraction can be demonstrated across lungs, splanchnic region, spleen, inferior limb and head. 3. No renin inactivation occurs in blood kept in vitro at 37°C for 3 h taken from anaesthetized dogs and from the anhepatic anephric dogs. 4. We suggest that the clearance of renin in the anhepatic anephric dog is due to extraction or inactivation of renin by tissues in general.

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.

Absence of Activation in Vitro of Renin in Rat Plasma

1982 ◽  
Vol 62 (4) ◽  
pp. 435-437 ◽  
Author(s):  
M. H. De Keijzer ◽  
A. P. Provoost ◽  
F. H. M. Derkx
Keyword(s):  
Human Plasma ◽  
Active Form ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Plasma Renin Concentration ◽  
Inactive Form ◽  
Inactive Renin

1. Rat plasma was subjected at 4°C to various treatments known to convert inactive renin into its active form in human plasma. 2. No statistical differences in plasma renin concentration were found when the levels after the various treatments were compared with that of untreated rat plasma. 3. It is concluded that, in contrast to human plasma, no inactive form of renin is present in rat plasma.

Modification of glycosylation of renin in sodium-depleted and captopril-treated rats

1989 ◽  
Vol 256 (6) ◽  
pp. E798-E804 ◽  
Author(s):  
S. Kim ◽  
M. Hosoi ◽  
M. Hiruma ◽  
F. Ikemoto ◽  
K. Yamamoto
Keyword(s):  
Half Life ◽  
Blood Circulation ◽  
Relative Proportion ◽  
Plasma Renin ◽  
Rat Plasma ◽  
Con A ◽  
Plasma Renin Concentration ◽  
Rat Renal Cortical Slices ◽  
Cortical Slices

Concanavalin A (con A) chromatography of rat plasma revealed the presence of three differently glycosylated forms of renin, including the con A unbound form (renin C), the loosely bound form (renin A), and the tightly bound form (renin B). Rat renal cortical slices in vitro secreted all these forms. They had a different half-life in the plasma after ligation of both renal artery and vein (half-life of 21 +/- 1, 14 +/- 3, and 35 +/- 4 min for renin A, B, and C, respectively). Thus differently glycosylated forms of renin are released from the kidney into the blood circulation and disappear, with a different half-life. Rats were sodium-depleted and captopril-treated (40-60 mg.kg-1.day-1) for 2 wk, and the effects of these treatments on relative proportions of renin A, B, and C were investigated. These treatments elevated plasma renin concentration approximately 60-fold (from 24 +/- 3 to 1,406 +/- 128 ng angiotensin I.h-1.ml-1; P less than 0.01), in association with an increase in the relative percent of renin C in the plasma from 22 +/- 2 to 39 +/- 3% (P less than 0.01). Moreover, the relative proportion of renin C released from the renal cortical slices was significantly higher in the treated than in the control rats (42 +/- 9 vs. 16 +/- 3% of secreted renin, respectively; P less than 0.02). These results show that the predominant release of renin C, with the longest half-life (35 min) in the plasma, contributes to the increased plasma renin concentration in sodium-depleted and captopril-treated rats.

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

Effect of linoleic acid infusion on blood pressure in normotensive and hypertensive rats

1989 ◽  
Vol 257 (2) ◽  
pp. H611-H617 ◽  
Author(s):  
S. R. Reddy ◽  
R. Talwalkar ◽  
J. Downs ◽  
T. A. Kotchen
Keyword(s):  
Blood Pressure ◽  
Linoleic Acid ◽  
Sodium Chloride ◽  
Enzymatic Activity ◽  
Plasma Renin ◽  
Sprague Dawley ◽  
Acid Infusion ◽  
High Sodium ◽  
Hypotensive Response

High dietary intake of linoleic acid lowers arterial pressure, and, in vitro, linoleic acid inhibits the enzymatic activity of renin. The purpose of the present study was 1) to evaluate the effect of intravenous infusion of linoleic acid on blood pressure in normotensive and hypertensive Sprague-Dawley rats and 2) to determine whether the hypotensive response to linoleic acid infusion is caused by inhibition of circulating renin. Blood pressure was decreased (P less than 0.01) by linoleic acid infusion in normotensive sodium chloride-deprived animals and in animals with two-kidney, one-clip hypertension. In contrast, linoleic acid infusion did not affect blood pressure in normotensive rats on a "normal" or high sodium chloride intake, in rats with deoxycorticosterone acetate (DOCA)-salt hypertension, and in anephric rats. In sodium chloride-deprived rats, the reduction of blood pressure by linoleic acid infusion was associated with increased plasma renin activity (P less than 0.05); serum angiotensin-converting enzyme activity was unchanged. The in vitro enzymatic activity of exogenous renin in plasma of anephric rats was not affected by linoleic acid infusion. In two-kidney, one-clip hypertensive animals, pretreatment with indomethacin did not alter the hypotensive response to linoleic acid. Thus, although linoleic acid infusion lowered blood pressure in high renin but not in low renin states, the reduction of blood pressure was not related to inhibition of circulating renin or to alterations of endogenous prostaglandin biosynthesis.

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.

scholarly journals Nonproportional changes in plasma renin concentration, renal renin content, and rat renin messenger RNA.

Hypertension ◽  
1985 ◽  
Vol 7 (6_pt_1) ◽  
pp. 855-859 ◽  
Author(s):  
N Nakamura ◽  
F Soubrier ◽  
J Menard ◽  
J J Panthier ◽  
F Rougeon ◽  
...  
Keyword(s):  
Messenger Rna ◽  
Plasma Renin ◽  
Plasma Renin Concentration ◽  
Renin Content

17α-HYDROXYLASE DEFICIENCY. A COMBINATION OF HYDROXYLATION DEFECT AND REVERSIBLE BLOCKADE IN ALDOSTERONE BIOSYNTHESIS

1979 ◽  
Vol 90 (3) ◽  
pp. 490-504 ◽  
Author(s):  
D. R. Rovner ◽  
J. W. Conn ◽  
E. L. Cohen ◽  
F. G. Berlinger ◽  
D. C. Kern ◽  
...  
Keyword(s):  
Plasma Concentration ◽  
Extracellular Fluid ◽  
Plasma Renin ◽  
Hydroxyl Group ◽  
Side Chain ◽  
Hydroxylase Deficiency ◽  
Resultant Increase

ABSTRACT We have studied the hormonal secretion and excretion patterns in a patient with the XX type of 17α-hydroxylase deficiency. In the untreated state, the patient's urine contained only those steroids which do not require 17-hydroxylation in their biosynthesis. Aldosterone was not produced in the patient and the metabolic product of its immediate precursor, 18-hydroxy-11-dehydro-tetrahydrocorticosterone, was excreted in markedly elevated amounts. This apparent complete block in 18 oxidation was reversible upon long-term ACTH suppression within 27 days. Direct in vitro incubation of the patient's adrenal gland removed at operation demonstrated, 1) the complete lack of 17α-hydroxylase activity, 2) the functional block in the ability to oxidize the hydroxyl group at the 18 methyl side chain. The addition of physiological concentrations of angiotensin to the incubation medium further showed, 3) angiotensin mildly stimulated the entire aldosterone biosynthetic pathway, 4) angiotensin directly stimulated the conversion of 18-hydroxycorticosterone to aldosterone. We propose that in this patient, 17-hydroxylase deficiency produced a decreased plasma concentration of cortisol, followed by stimulation of deoxycorticosterone production by ACTH. The resultant increase in extracellular fluid volume suppressed plasma renin activity. This resulted in a low plasma concentration of angiotensin II which directly suppressed oxidation of 18-hydroxycorticosterone to aldosterone. This defect has been called corticosterone methyl oxidase defect type 2.

scholarly journals Heightened Cardiovascular Risk in Hypertension Associated With Renin‐Independent Aldosteronism Versus Renin‐Dependent Aldosteronism: A Collaborative Study

2021 ◽  
Author(s):  
Jinbo Hu ◽  
Hang Shen ◽  
Peiqi Huo ◽  
Jun Yang ◽  
Peter J Fuller ◽  
...  
Keyword(s):  
Collaborative Study ◽  
Challenge Test ◽  
Plasma Renin ◽  
Excretion Ratio ◽  
Aldosterone Secretion ◽  
Cvd Risk ◽  
Baseline Serum ◽  
Plasma Renin Concentration ◽  
Serum Aldosterone ◽  
Urinary Potassium

Background While both renin‐dependent and renin‐independent aldosterone secretion contribute to aldosteronism, their relative associations with cardiovascular disease (CVD) risk has not been investigated. Methods and Results A total of 2909 participants from the FOS (Framingham Offspring Study) with baseline, serum aldosterone concentration, and plasma renin concentration who attended the sixth examination cycle and were followed up until 2014 and who were free of CVD were included. We further recruited 2612 hypertensive participants from the CONPASS (Chongqing Primary Aldosteronism Study). Captopril challenge test was performed to confirm renin‐dependent or ‐independent aldosteronism in CONPASS. Among 1433 hypertensive subjects of FOS, when compared with those with serum aldosterone concentration <10 ng dL −1 (normal aldosterone), participants who had serum aldosterone concentration ≥10 ng dL −1 and plasma renin concentration ≤15 mIU L −1 (identified as renin‐independent aldosteronism) showed a higher risk of CVD (hazard ratio, 1.40 [95% CI, 1.08–1.82]), while those who had serum aldosterone concentration ≥10 ng dL −1 and plasma renin concentration >15 mIU L −1 (identified as renin‐dependent aldosteronism) showed an unchanged CVD risk. In CONPASS, renin‐independent aldosteronism carried a significantly higher risk of CVD than normal aldosterone (odds ratio, 2.57 [95% CI, 1.13–5.86]), while the CVD risk remained unchanged in renin‐dependent aldosteronism. Elevation of the urinary potassium‐to‐sodium excretion ratio, reflective of mineralocorticoid receptor activity, was only observed in participants with renin‐independent aldosteronism. Conclusions Among patients with hypertension, renin‐independent aldosteronism is more closely associated with CVD risk than renin‐dependent aldosteronism.

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