Urinary Protein Excretion in Normal Individuals: Diurnal Changes, Influence of Orthostasis and Relationship to the Renin-Angiotensin System

2015 ◽  
pp. 143-150 ◽  
Author(s):  
B. A. C. van Acker ◽  
M. K. J. Stroomer ◽  
M. A. H. E. Gosselink ◽  
G. C. M. Koomen ◽  
M. G. Koopman ◽  
...  
Keyword(s):  
Renin Angiotensin System ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Diurnal Changes ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Protein Excretion ◽  
Normal Individuals

Differential evolution of blood pressure and renal lesions after RAS blockade in Lyon hypertensive rats

2002 ◽  
Vol 283 (5) ◽  
pp. R1041-R1045 ◽  
Author(s):  
Delphine Bertram ◽  
Nelly Blanc-Brunat ◽  
Jean Sassard ◽  
Ming Lo
Keyword(s):  
Blood Pressure ◽  
Antihypertensive Effect ◽  
Enzyme Inhibitor ◽  
Renin Angiotensin System ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Histological Changes ◽  
Angiotensin System ◽  
Renal Lesions ◽  
Protein Excretion

The present work aimed to assess, in Lyon hypertensive (LH) rats, whether an early and prolonged inhibition of the renin-angiotensin system (RAS) could result in a blood pressure (BP) lowering and nephroprotection that persist after its withdrawal. Male LH rats received orally from 3 to 12 wk of age either an angiotensin-converting enzyme inhibitor perindopril at the doses of 0.4 and 3 mg · kg−1· day−1or an AT1receptor antagonist losartan at the dose of 10 mg · kg−1· day−1. BP, histological changes in the kidney, and urinary protein excretion were examined during and 10 wk after cessation of the treatments. Both perindopril and losartan decreased BP, prevented renal lesions, and limited urinary protein excretion. After cessation of the treatment, BP returned to the level of never-treated LH rats in rats having received 3 mg · kg−1· day−1of perindopril while it remained slightly lower in those treated with 0.4 mg · kg−1· day−1of perindopril or with losartan. This lack of marked persistent antihypertensive effect contrasted with a durable decrease in urinary protein excretion and improvement of the renal histological lesions. In conclusion, it is possible to separate the BP-lowering effects of RAS blockade from those on glomerulosclerosis and urinary protein excretion.

Abstract P031: Reduced Augmentation Of The Intrarenal Renin-angiotensin System (ras), Lower Systolic Blood Pressure, And Preserved Renal Function In Female Compared To Male Rats With Unilateral Renal Artery Stenosis

Hypertension ◽  
2020 ◽  
Vol 76 (Suppl_1) ◽  
Author(s):  
Annie L Bell ◽  
Weijian A Shao ◽  
Akemi Katsurada ◽  
Ryosuke Sato ◽  
L Gabriel G NAVAR
Keyword(s):  
Renal Function ◽  
Renal Artery ◽  
Renal Artery Stenosis ◽  
Renin Angiotensin System ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Artery Stenosis ◽  
Female Rats ◽  
Male Rats ◽  
Protein Excretion

Despite growing evidence of sex differences in the progression of hypertension, there are no guidelines that differentiate treatment between men and women. Intrarenal renin-angiotensin system (RAS) activation and tissue injury in 2-kidney, 1-clip (2K1C) hypertensive rats have been characterized in previous studies of male but not female rats. To evaluate possible sex differences in response to renovascular hypertension, urinary angiotensinogen (uAGT) excretion, systolic blood pressure (BP), urinary protein excretion, and renal function were assessed in female rats.Female (n=8) and male (n=6) rats underwent placement of a 0.2 mm clip on the left renal artery to simulate unilateral renal artery stenosis. BP was measured by tail-cuff plethysmography, and clearance studies were conducted in anesthetized rats to assess renal function. Urine protein concentration was determined by pyrogallol red method. uAGT was measured by ELISA as an index of intrarenal RAS activity. Systolic BP increased from 120±1 to 176±8 mmHg, and urinary protein excretion reached 20.2±5.6 mg/day in female rats. Although uAGT excretion increased from 13.2±7.7 ng/day to 74.1±29.9 ng/day in female rats, male rats had a significantly higher uAGT excretion of 1572.6±750 ng/day. Nonclipped kidneys exhibited more uAGT excretion compared to clipped kidneys, consistent with previous findings in males. Although 2K1C female rats demonstrate significantly lower renal function than sham females, they show more preserved renal function than male rats. Female rats also demonstrate significantly lower increases in systolic BP and urinary protein excretion compared to male rats. The data support substantial sex-dependent differences in renal responses to unilateral renal artery stenosis. The results show substantial increases in systolic BP, uAGT, and urinary protein excretion and decreased renal function after renal artery clipping in females, but the magnitude of the changes is markedly lower than in males. Nonclipped kidneys of both sexes exhibit greater uAGT excretion than clipped kidneys. Notably, females show less augmentation of the intrarenal RAS compared to male rats in renovascular hypertension.

scholarly journals Angiotensin II modulates glomerular capillary permselectivity in rat isolated perfused kidney.

1996 ◽  
Vol 7 (5) ◽  
pp. 653-660 ◽  
Author(s):  
R Lapinski ◽  
N Perico ◽  
A Remuzzi ◽  
F Sangalli ◽  
A Benigni ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Excretion Rate ◽  
Rat Kidney ◽  
Renin Angiotensin System ◽  
Urinary Protein Excretion ◽  
Urinary Protein ◽  
Converting Enzyme Inhibitors ◽  
Glomerular Capillary ◽  
Protein Excretion ◽  
Fractional Clearance

Studies in experimental animals and humans have documented that inhibition of the renin-angiotensin system by angiotensin-converting enzyme inhibitors reduces urinary protein excretion rate and retards the development of renal injury. Here we sought to investigate whether angiotensin II (All) modified the size-selective properties to macromolecules of the glomerular capillary barrier in isolated perfused rat kidney preparation. Compared with basal values, continuous All infusion into the renal artery at the rate of 3 or 8 ng/min, but not at 0.6 ng/min, induced a progressive and significant increase in urinary protein excretion rate. Evaluation of the sieving properties of the glomerular barrier by fractional clearance of polydisperse Ficoll showed that All significantly enhanced the filtration of tracer molecules of radil > or = 34A. All-induced changes in urinary protein excretion rate and in Ficoll fractional clearance were completely prevented by pretreatment with the specific All Type 1 receptor antagonist SR 47436.

Increased urinary protein excretion in the “normal” range is associated with increased renin-angiotensin system activity

2012 ◽  
Vol 302 (5) ◽  
pp. F526-F532 ◽  
Author(s):  
David D. M. Nicholl ◽  
Brenda R. Hemmelgarn ◽  
Tanvir C. Turin ◽  
Jennifer M. MacRae ◽  
Daniel A. Muruve ◽  
...  
Keyword(s):  
Arterial Stiffness ◽  
Renin Angiotensin System ◽  
Applanation Tonometry ◽  
Ang Ii ◽  
Healthy Individuals ◽  
Normal Range ◽  
Indirect Measure ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Protein Excretion

Increased levels of albuminuria and proteinuria, both linked to augmented renin-angiotensin system (RAS) activity, are associated with adverse kidney and cardiovascular events. However, the relationship between variations in urinary albumin excretion (UAE) and total protein excretion (UTPE) in the normal range and RAS activity is unclear. We examined the association between UAE and UTPE and the hemodynamic response to angiotensin II (ANG II) challenge, a well-accepted indirect measure of RAS activity, in healthy individuals with normal UAE and UTPE. Forty subjects (15 men, 25 women; age 38 ± 2 yr; UAE, 3.32 ± 0.55 mg/day; UTPE, 56.8 ± 3.6 mg/day) were studied in high-salt balance. Blood pressure (BP), arterial stiffness determined by applanation tonometry, and circulating RAS components were measured at baseline and in response to graded ANG II infusion. The primary outcome was the BP response to ANG II challenge at 30 and 60 min. UAE was associated with a blunted diastolic BP response to ANG II infusion (30 min, P = 0.005; 60 min, P = 0.17), a relationship which remained even after adjustment (30 min, P < 0.001; 60 min, P = 0.035). Similar results were observed with UTPE (30 min, P = 0.031; 60 min, P = 0.001), even after multivariate analysis (30 min, P = 0.008; 60 min, P = 0.001). Neither UAE nor UTPE was associated with systolic BP, circulating RAS components, or arterial stiffness responses to ANG II challenge. Among healthy individuals with UAE and UTPE in the normal range, increased levels of these measures were independently associated with a blunted diastolic BP response to ANG II, indicating increased vascular RAS activity, which is known to be deleterious to both renal and cardiac function.

Studies on the Renin-Angiotensin System in a Kininogen-Deficient Individual

1983 ◽  
Vol 65 (2) ◽  
pp. 121-126 ◽  
Author(s):  
Patrick Y. Wong ◽  
Gordon H. Williams ◽  
Robert W. Colman
Keyword(s):  
Angiotensin Ii ◽  
Plasma Renin Activity ◽  
Renin Angiotensin System ◽  
Plasma Renin ◽  
Renin Activity ◽  
Dietary Sodium ◽  
Sodium Balance ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Normal Individuals

1. The physiological responses of the renin-angiotensin system were studied in an individual with kininogen deficiency (patient 1) with absent plasma bradykinin and markedly impaired prekallikrein conversion into kallikrein. After sodium depletion, patient 1 had a low plasma renin activity (1.4 pmol of ANG I h−1 ml−1) and a low angiotensin II concentration (36 pg/ml) compared with values in 11 normal individuals (4.0 ± 0.94 pmol of ANG I h−1 ml−1) and 63 ±6 pg/ml respectively). 2. Unlike normal individuals, in the kininogen-deficient subject there was no significant fall of renin activity or angiotensin II after dietary sodium repletion. Intravenous sodium repletion also failed to further decrease plasma renin activity or angiotensin II. 3. The usual two- to three-fold rise in plasma renin activity and angiotensin II observed in normal subjects on assumption of the upright posture after ingestion of 200 mg of sodium/day failed to occur in the kininogen-deficient individual. 4. These data in vivo are in agreement with observations in vitro that once plasma kallikrein forms it may be important in converting prorenin into renin. In the absence of kininogen, activation of prekallikrein to kallikrein is grossly defective, which may in part account for the diminished response of the renin-angiotensin system to changes in sodium balance and posture.

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