Long-term Regulation of Arterial Pressure, Glomerular Filtration and Renal Sodium Reabsorption by Angiotensin II in Dogs

1980 ◽  
Vol 59 (s6) ◽  
pp. 87s-90s ◽  
Author(s):  
J. E. Hall ◽  
A. C. Guyton ◽  
M. J. Smith ◽  
T. G. Coleman
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Sodium Balance ◽  
Sodium Reabsorption ◽  
Filtration Fraction ◽  
Plasma Aldosterone Concentration

1. This study was designed to quantify the role of angiotensin II in determining the chronic relationships between arterial pressure, renal haemodynamics and sodium excretion. 2. In six control dogs sodium balance was achieved during chronic increases in sodium intake from 5 to 495 mmol/day with small increases in arterial pressure (7mmHg), moderate increases in glomerular filtration rate (19%) and decreases in filtration fraction. Similar increases in sodium intake in dogs whose circulating levels of angiotensin II were fixed, due to a constant intravenous infusion of 4.85 pmol of angiotensin II min−1 kg−1, caused large increases in arterial pressure (42%), glomerular filtration rate (31%), filtration fraction and calculated renal sodium reabsorption above control. In six dogs whose angiotensin II formation was blocked by SQ 14 225, sodium balance at intakes of 5–80 mmol/day occurred at reduced arterial pressure, glomerular filtration rate, filtration fraction and sodium reabsorption although plasma aldosterone concentration was not substantially different from that in control dogs. At sodium intakes above 240 mmol/day arterial pressure was not altered by SQ 14 225. 3. These data indicate that during chronic variations in sodium intake angiotensin II plays a major role, independently of changes in plasma aldosterone concentration, in allowing sodium balance without large fluctuations in glomerular filtration rate or arterial pressure. The mechanism whereby angiotensin II conserves sodium chronically is through increased sodium reabsorption, since steady-state sodium reabsorption was increased by angiotensin II and decreased by SQ 14 225.

Site of Action of Angiotensin and other Vasoconstrictors on the Kidney

1971 ◽  
Vol 49 (6) ◽  
pp. 608-612 ◽  
Author(s):  
D. Regoli ◽  
R. Gauthier
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Krebs Solution ◽  
Angiotensin I ◽  
Filtration Fraction ◽  
Site Of Action

Angiotensin II, angiotensin I, adrenaline, or noradrenaline was infused in rabbit kidneys isolated and perfused with oxygenated Krebs solution. Adrenaline increased the perfusion pressure and slightly decreased the filtration fraction and the glomerular filtration rate. Angiotensins had similar effects on the perfusion pressure, but significantly increased filtration fraction and glomerular filtration rate.It is suggested that adrenaline acts on the afferent, while angiotensins II and I constrict the efferent, glomerular artery.

Angiotensin II binding to renal glomeruli from sodium-loaded and sodium-depleted rats

1976 ◽  
Vol 230 (5) ◽  
pp. 1187-1193 ◽  
Author(s):  
M Beaufils ◽  
J Sraer ◽  
C Lepreux ◽  
R Ardaillou
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Dissociation Constants ◽  
Sodium Balance ◽  
Renal Glomeruli ◽  
Receptor Sites ◽  
Specificity Of Binding ◽  
Isolated Rat

125I-labeled angiotensin II (125I-labeled AII) and [3H]angiotensin II ([3H]AII) bind specifically to isolated rat glomeruli. Three groups of receptor sites could be defined by the KD value (7.1 +/- 0.3 X 10(-11, 3.4 +/- 0.2 X 10(-10), and 1.6 X 10(-9) M, respectively) and the number of receptor sites (11.6 +/- 1.2, 29.4 +/- 3.9, and 113.8 +/- 3.8 fmol/mg glomerular protein, respectively). Both association and dissociation constants for 125I-labeled AII were greater than those for [3H]AII, but their ratio (KD) remained unchanged. Specificity of binding to these three groups of receptor sites was demonstrated by the following: 1) inhibition of binding of labeled AII by unlabeled hormone or by antagonists; and 2) reversibility of binding, independent of either hormone or receptor degradation. Binding was increased in glomerular preparations from acutely and chronically sodium-loaded rats, compared with glomerular preparations from acutely and chronically sodium-depleted rats. This change in binding resulted from both a change in the number of receptor sites and modification of the affinity of AII for its receptors. KD was higher in preparations from sodium-depleted rats (12.9 +/- 3.3 and 14.6 +/- 3.9 X 10(-11) M in chronically and acutely depleted rats, respectively) than in those from sodium-loaded rats (2.7 +/- 0.2 and 3.9 +/- 1 X 10(-11) M in chronically and acutely sodium-loaded rats, respectively). Changes in the binding of AII to its glomerular receptors could play a role in the adaptation of glomerular filtration rate to the sodium balance.

Unimpaired excretion of an acute salt load in conscious hypoproteinaemic dogs

1988 ◽  
Vol 75 (3) ◽  
pp. 271-276 ◽  
Author(s):  
J. A. Joles ◽  
H. A. Koomans ◽  
P. Boer ◽  
E. J. Dorhout Mees
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Protein ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Isotonic Saline ◽  
Fractional Excretion ◽  
Sodium Reabsorption ◽  
Filtration Fraction ◽  
Fractional Excretion Of Sodium

1. The role of hypoproteinaemia in the sodium retention seen in conditions such as the nephrotic syndrome is incompletely known. 2. To define the influence of severe hypoproteinaemia on kidney function, we studied the effect of an intravenous infusion of an isotonic saline load (133 mmol of sodium), as 1 litre of Ringer lactate solution, on sodium excretion and renal haemodynamics in conscious dogs before and after reduction of plasma protein from 68 ± 3 to 36 ±2 g/l by repeated plasmapheresis and a low protein diet. 3. During hypoproteinaemia, 2 days after a period of plasmapheresis, glomerular filtration rate and effective renal plasma flow were lower than in the control study. After the sodium load, both rose to values nearly identical with the pre-infusion levels found in normoproteinaemia, the filtration fraction remaining unchanged. This contrasted with the rise in filtration fraction after expansion in normoproteinaemia, where filtration fraction increased from 32 to 39% due to a rise in glomerular filtration rate. 4. After expansion, natriuresis rose to similar levels in normoproteinaemia (0.18 ±0.06 mmol/min) and hypoproteinaemia (0.20 ± 0.06 mmol/min), and increments in fractional excretion of sodium, potassium and chloride were also similar. However, baseline excretion was higher in the hypoproteinaemic dogs due to their overhydrated condition in this period immediately after plasmapheresis. 5. The fractional excretion of lithium, an alleged marker of proximal tubular sodium reabsorption, rose to comparable levels. 6. Hence, both the increase in filtration and decrease in reabsorption of sodium after an isotonic saline load are not affected by severe reduction in plasma protein concentration. Apparently, the pathways to augment natriuresis after acute expansion function normally in hypoproteinaemia.

scholarly journals Individual renal hemodymamic response to chronic angiotensin II receptor bloc­kade and the influence on the renin-angiotensin system gene polymorphisms

2010 ◽  
Vol 63 (9-10) ◽  
pp. 630-637
Author(s):  
Tamara Dragovic ◽  
Boris Ajdinovic ◽  
Vesna Ilic ◽  
Zvonko Magic ◽  
Zoran Andjelkovic ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Filtration Fraction ◽  
Renal Vascular ◽  
Losartan Treatment

Introduction. Our study was aimed at determining whether the polymorphism of genes for different components of the renin-angiotensin-aldosterone system could influence the renal hemodynamic response to losartan treatment. Material and method. The study included 35 patients with type 1 diabetes mellitus and persistent albuminuria, genotyped for the 1166 A/C polymorphism gene for the angiotensin II type 1 receptor and I/D polymorphism of the angiotensin-converting enzyme gene. The participants were divided into groups according to the combinations of A or C allele: AA, AC, CC; and according to the combinations of I or D allele: II, ID and DD genotype. The patients received losartan therapy for 12 weeks. The renal hemodynamic measurements were determined at baseline and after the examination period. Results. Losartan therapy significantly reduced the filtration fraction from the baseline by 0.018?0.024 (p=0.012) only in the AC genotype. The glomerular filtration rate remained unchanged in all genotype groups. A significant increase in the effective renal plasma flow was obtained only in AC genotype (544?88 vs 575?90ml/min; p=0.02), while significant reductions in the renal vascular resistance were found in AA group (115?25 vs 95?21 mmHgx1-1xmin-1; p=0.001) and in AC group (118?30 vs 101?28 mmHgx1-1xmin-1; p=0.001). A significant reduction of the glomerular filtration rate by 8?10 ml/min was obtained only in the DD genotype (p=0.016), and only the DD genotype achieved a significant reduction of the filtration fraction by 0.019?0,022 (p=0.008). The most pronounced increase of the effective renal plasma flow was found only in the ID genotype (536 ?75 vs 591?63 ml/min; p=0.01). The reduction of the renal vascular resistance was independent of ACE gene polymorphism. Conclusion. Our study shows that individual renal vascular response to losartan treatment in diabetic patients with persistent albuminuria, could be influenced by genetic polymorphisms.

Control of glomerular filtration rate: role of intrarenally formed angiotensin II

1984 ◽  
Vol 246 (6) ◽  
pp. F897-F906 ◽  
Author(s):  
P. R. Kastner ◽  
J. E. Hall ◽  
A. C. Guyton
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Venous Blood ◽  
Control Level ◽  
Renin Angiotensin System ◽  
Ang Ii ◽  
Filtration Fraction

This study was designed to investigate the role of intrarenally formed angiotensin II (ANG II) in controlling glomerular filtration rate (GFR) during reduction of renal artery pressure (RAP). The experimental design prevented renin released by the kidney from entering the systemic circulation and therefore prevented changes in circulating ANG II from influencing GFR control. In dogs with only a functional intrarenal renin-angiotensin system (RAS), GFR and renal blood flow (RBF) were not significantly altered by RAP reduction to 70 mmHg. After blockade of intrarenal ANG II formation with SQ 14225, reduction of RAP to 70 mmHg decreased GFR and filtration fraction to 75.6 +/- 7.0 and 59.0 +/- 4.1% of control, respectively, while RBF remained at 129.3 +/- 8.8% of control. Calculated efferent arteriolar resistance decreased considerably more when RAP was reduced after SQ 14225, whereas preglomerular resistance decreased to about the same level as observed prior to SQ 14225 infusion. After return of endogenously produced ANG II by recirculation of the renal venous blood or after infusion of ANG II (following SQ 14225) at a rate that restored RBF to the control level (with RAP held at 70 mmHg in each case), GFR, filtration fraction, and calculated efferent resistance were restored to control levels, but preglomerular resistance did not change. These results suggest that intrarenal ANG II formation plays an important role in maintaining GFR during reductions in RAP by constricting efferent arterioles.(ABSTRACT TRUNCATED AT 250 WORDS)

Direct hemodynamic effect of insulin in the isolated perfused kidney

1989 ◽  
Vol 257 (4) ◽  
pp. F580-F585 ◽  
Author(s):  
A. J. Cohen ◽  
D. M. McCarthy ◽  
J. S. Stoff
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Hemodynamic Effect ◽  
Sodium Reabsorption ◽  
Ang Ii ◽  
Isolated Perfused Kidney ◽  
Vasodilatory Effect ◽  
Natriuretic Effect

The hemodynamic effect of insulin was examined in isolated perfused kidneys. Experiments were designed to study the effect of the hormone on basal hemodynamics and in the presence of angiotensin II (ANG II). Physiological insulin concentrations caused both renal vasodilation and increased glomerular filtration rate (GFR) during basal perfusion periods and attenuated the vasoconstrictor action of ANG II while limiting the ANG II-induced reduction of GFR. Insulin also increased fractional sodium reabsorption and diminished the natriuretic effect of ANG II. The addition of insulin to perfusions in which ANG II was infused from the start caused renal vasodilation, although supraphysiological concentrations were required. Kidneys perfused with hyperoncotic albumin to prevent filtration similarly demonstrated a vasodilatory effect of insulin that did not require glomerular filtration. Inhibition of prostaglandin (PG) synthesis with indomethacin prevented the vasodilatory effects of insulin. These data support the hypothesis that insulin causes renal vasodilation by a PG-dependent process.

Effect of Proportional Reduction of Sodium Intake on the Adaptive Increase in Glomerular Filtration Rate/Nephron and Potassium and Phosphate Excretion in Chronic Renal Failure in the Rat

1975 ◽  
Vol 49 (3) ◽  
pp. 193-200 ◽  
Author(s):  
C. H. Espinel
Keyword(s):  
Renal Failure ◽  
Glomerular Filtration Rate ◽  
Chronic Renal Failure ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Sodium Intake ◽  
Dietary Sodium ◽  
Control Group ◽  
Phosphate Excretion

1. The influence of dietary sodium intake on the glomerular filtration rate (GFR/nephron) and potassium and phosphate excretion was examined at three stages of progressive chronic renal failure produced in rats by sequential partial nephrectomies. 2. The adaptive increased sodium excretion per nephron in the control group receiving a constant sodium intake did not occur in the experimental group that had a gradual reduction of dietary sodium in direct proportion to the fall in GFR. 3. Despite the difference in sodium excretion, the increase in GFR/nephron, the daily variation in the amount of potassium and phosphate excreted, the increase in potassium and phosphate excretion per unit nephron, and the plasma potassium and phosphate concentrations were the same in the two groups. 4. The concept of ‘autonomous adaptation’ in chronic renal failure is presented.

Global REACH 2018: Volume regulation in high-altitude Andeans with and without chronic mountain sickness

2021 ◽  
Author(s):  
Andrew R. Steele ◽  
Michael M. Tymko ◽  
Victoria L. Meah ◽  
Lydia L Simpson ◽  
Christopher Gasho ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Plasma Renin Activity ◽  
High Altitude ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Plasma Renin ◽  
Renin Activity ◽  
Chronic Mountain Sickness ◽  
Plasma Aldosterone Concentration ◽  
Mountain Sickness

The high-altitude maladaptation syndrome known as chronic mountain sickness (CMS) is characterized by polycythemia and is associated with proteinuria despite unaltered glomerular filtration rate. However, it remains unclear if indigenous highlanders with CMS have altered volume regulatory hormones. We assessed N-terminal pro-B-type natriuretic peptide (NT pro-BNP), plasma aldosterone concentration, plasma renin activity, kidney function (urinary microalbumin, glomerular filtration rate), blood volume, and estimated pulmonary artery systolic pressure (ePASP), in Andean males without (n=14; age=39±11) and with (n=10; age=40±12) CMS at 4330 meters (Cerro de Pasco, Peru). Plasma renin activity (non-CMS: 15.8±7.9 vs. CMS: 8.7±5.4 ng/ml; p=0.025) and plasma aldosterone concentration (non-CMS: 77.5±35.5 vs. CMS: 54.2±28.9 pg/ml; p=0.018) were lower in highlanders with CMS compared to non-CMS, while NT pro-BNP was not different between groups (non-CMS: 1394.9±214.3 vs. CMS: 1451.1±327.8 pg/ml; p=0.15). Highlanders had similar total blood volume (non-CMS: 90±15 vs. CMS: 103±18 ml • kg-1; p=0.071), but Andeans with CMS had greater total red blood cell volume (non-CMS: 46±10 vs. CMS 66±14 ml • kg-1; p<0.01) and smaller plasma volume (non-CMS 43±7 vs. CMS 35±5 ml • kg-1; p=0.03) compared to non-CMS. There were no differences in ePASP between groups (non-CMS 32±9 vs. CMS 31±8 mmHg; p=0.6). A negative correlation was found between plasma renin activity and glomerular filtration rate in both groups (group: r=-0.66; p<0.01; non-CMS: r=-0.60; p=0.022; CMS: r=-0.63; p=0.049). A smaller plasma volume in Andeans with CMS may indicate an additional CMS maladaptation to high-altitude, causing potentially greater polycythemia and clinical symptoms.

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