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.

Interaction between angiotensin II and nitric oxide in control of renal hemodynamics in conscious dogs

1994 ◽  
Vol 267 (6) ◽  
pp. R1472-R1478 ◽  
Author(s):  
A. M. Alberola ◽  
F. J. Salazar ◽  
T. Nakamura ◽  
J. P. Granger
Keyword(s):  
Nitric Oxide ◽  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Nitric Oxide Synthesis ◽  
Afferent Arterioles ◽  
Renal Vascular

Recent in vitro studies have provided evidence that the vasoconstrictor actions of angiotensin II on afferent arterioles are enhanced by nitric oxide synthesis inhibition. Although these studies suggest that nitric oxide may play a role in protecting the afferent arterioles from angiotensin II-induced vasoconstriction, the importance of this interaction in the regulation of glomerular filtration rate and renal blood flow in the intact, conscious animal is not known. The objective of the present study was to determine the role of nitric oxide in modulating the renal hemodynamic and excretory effects of angiotensin II. Angiotensin II was infused at rates of 0.5, 1.0, and 2.0 micrograms.kg-1.min-1 intrarenally in conscious, chronically instrumented dogs in both the presence and absence of nitric oxide synthesis inhibition by continuous intrarenal infusion of NG-nitro-L-arginine methyl ester (3 micrograms.kg-1.min-1). At a dose of 0.5 micrograms.kg-1.min-1, angiotensin II decreased renal plasma flow by 19%, while having no effect on glomerular filtration rate in control dogs. In contrast, angiotensin II decreased renal plasma flow by 54%, glomerular filtration rate by 40%, and increased renal vascular resistance by 125% in the presence of intrarenal nitric oxide synthesis blockade. At doses of 1.0 and 2.0 micrograms.kg-1.min-1, angiotensin II reduced renal plasma flow by 36 and 45%, glomerular filtration rate by 17 and 23%, and increased renal vascular resistance by 80 and 120%, respectively, in control dogs.(ABSTRACT TRUNCATED AT 250 WORDS)

Angiotensin II modulates the intrarenal effects of atrial natriuretic peptide

1988 ◽  
Vol 255 (3) ◽  
pp. F545-F551
Author(s):  
H. M. Siragy ◽  
N. E. Lamb ◽  
C. E. Rose ◽  
M. J. Peach ◽  
R. M. Carey
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Atrial Natriuretic Peptide ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Systemic Effects ◽  
Ang Ii ◽  
Renal Effects

The mechanism by which atrial natriuretic peptide (ANP) increases renal water and solute excretion is not fully understood. We studied the renal effects of ANP and angiotensin II (ANG II) separately and together in uninephrectomized conscious dogs (n = 7) in sodium metabolic balance (80 meq/day). Exogenous ANG II and ANP were without measurable systemic effects as demonstrated by absence of changes in blood pressure, plasma aldosterone concentration, and plasma renin activity. The quantity of ANG II that had significant renal effects that were without measurable systemic effects was 0.2 pmol.kg-1.min-1. Three infusion rates of ANP had significant renal effects (1, 10, and 20 pmol.kg-1.min-1). These quantities of ANP caused significant diuresis, natriuresis, kaliuresis, and increased glomerular filtration rate without significant changes in renal plasma flow. ANG II alone caused significant antidiuresis, antinatriuresis, and decreased glomerular filtration rate and renal plasma flow. When ANG II and ANP were given together, no change in urinary flow rate, urinary sodium or potassium excretion, or renal plasma flow was observed, whereas glomerular filtration rate increased. Filtration fraction increased significantly with ANG II and ANP separately and together. Intrarenal ANP prevents the ANG II-induced decrement in urinary sodium excretion and urine flow rate. ANP may play an important role in escape from the sodium-retaining action of intrarenal ANG II.

Glomerular binding and contractile response to angiotensin II in rats with chronic experimental cirrhosis of the liver

1991 ◽  
Vol 80 (2) ◽  
pp. 143-147 ◽  
Author(s):  
Luis M. Villamediana ◽  
Mercedes Velo ◽  
Ana Olivera ◽  
Luis Hernando ◽  
Carlos Caramelo ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Angiotensin Ii ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Contractile Response ◽  
Renal Plasma Flow ◽  
Cross Sectional Area ◽  
Sectional Area ◽  
Cross Sectional

1. The effects of angiotensin II on glomerular filtration rate and renal plasma flow were studied in surgically instrumented conscious control and cirrhotic rats. In addition, angiotensin II binding and the contractile response to angiotensin II were studied in glomeruli isolated from cirrhotic and control rats. 2. Cirrhotic rats had a higher glomerular filtration rate and a higher renal plasma flow than control animals. A non-pressor dose of angiotensin II induced small but significant decreases in glomerular filtration rate and renal plasma flow in both control and cirrhotic rats, the effect on renal plasma flow being the most pronounced. 3. Plasma renin and aldosterone concentrations were similar in control and cirrhotic rats. 4. The cross-sectional area of glomeruli from cirrhotic rats was 42% greater than that of glomeruli from control animals. Angiotensin II (10−9 mol/l) decreased the cross-sectional area of glomeruli from control animals by 6.4 ± 0.9% and of glomeruli from cirrhotic rats by 6.6 ± 0.8% (P = not significant for comparison between control and cirrhotic animals). 5. There were no differences between control and cirrhotic rats in the affinity of angiotensin II for its glomerular receptors. However, the angiotensin II receptor density was higher in cirrhotic than in control rats, thereby producing an increased total angiotensin II binding in cirrhotic rats. 6. Since no functional differences between control and cirrhotic animals were present in the response to angiotensin II, even though angiotensin II binding was increased, a post-receptor blockade of the angiotensin II signal could be present in cirrhotic rats.

scholarly journals Tubular Secretion Markers, Glomerular Filtration Rate, Effective Renal Plasma Flow, and Filtration Fraction in Healthy Adolescents

2020 ◽  
Vol 2 (5) ◽  
pp. 670-672
Author(s):  
Jesse C. Seegmiller ◽  
Brian J. Wolfe ◽  
Nansy Albtoush ◽  
Isabella Melena ◽  
Susan P. Gross ◽  
...  
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Tubular Secretion ◽  
Effective Renal Plasma Flow ◽  
Filtration Fraction

Evidence for endothelin-induced renal vasoconstriction independent of ETA receptor activation

1993 ◽  
Vol 264 (1) ◽  
pp. R222-R226 ◽  
Author(s):  
D. M. Pollock ◽  
T. J. Opgenorth
Keyword(s):  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Vascular Resistance ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Renal Vascular Resistance ◽  
Renal Vascular

Experiments were designed to examine the role of endothelin (ET) receptors, specifically ETA receptors, in mediating the renal vasoconstrictor effects of ET-1 in anesthetized Sprague-Dawley rats. Intravenous infusion of ET-1 at 25 pmol.kg-1 x min-1 for 60 min produced a significant increase in mean arterial pressure (20 +/- 7%) and decreases in renal plasma flow (-60 +/- 6%) and glomerular filtration rate (-47 +/- 6%). Renal vascular resistance was significantly increased from 17 +/- 1 mmHg.ml-1 x min.g kidney wt during control period to 54 +/- 11 mmHg.ml-1 x min.g kidney wt during the experimental period. A second group of rats was infused with both ET-1 and the specific ETA receptor antagonist BQ-123 (0.1 mg.kg-1 x min-1). ET-1-induced increases in mean arterial pressure were completely blocked by BQ-123 (the average change was -7 +/- 4%). However, the renal vasoconstrictor effects of ET-1 were not affected by the antagonist, since renal plasma flow and glomerular filtration rate were again significantly reduced (-54 +/- 4 and -56 +/- 6%, respectively). Once again, renal vascular resistance was significantly increased from 16 +/- 2 mmHg.ml-1 x min.g kidney wt during the control period to 33 +/- 5 mmHg.ml-1 x min.g kidney wt during the experimental period. In a third group, infusion of BQ-123 alone produced a significant decline in mean arterial pressure (-13 +/- 2%), with no significant changes in renal plasma flow or glomerular filtration rate, thus producing a significant decrease in renal vascular resistance (15 +/- 1 vs. 11 +/- 2 mmHg.ml-1 x min.g kidney wt).(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals RENAL FUNCTION DURING CHRONIC ANEMIA IN MAN

Blood ◽  
1947 ◽  
Vol 2 (2) ◽  
pp. 192-202 ◽  
Author(s):  
STANLEY E. BRADLEY ◽  
GERALDINE P. BRADLEY
Keyword(s):  
Blood Flow ◽  
Renal Function ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Plasma Flow ◽  
Filtration Rate ◽  
Normal Values ◽  
Renal Plasma Flow ◽  
Filtration Fraction ◽  
Chronic Anemia

Abstract 1. Renal function has been studied quantitatively in 15 patients with chronic anemia, 8 of whom were proved to have pernicious anemia. In 7 the anemia was secondary to chronic blood loss, iron deficiency, paroxysmal nocturnal hemoglobinuria, and leukemia. The effective renal plasma flow and glomerular filtration rate were measured by clearance technics; and tubular function, by saturation methods (diodrast Tm and glucose Tm). 2. The effective renal plasma flow, the glomerular filtration rate, and the filtration fraction (percentage of plasma filtered at the glomerulus) were reduced slightly below the normal values in most subjects. The effective renal whole blood flow was always greatly reduced, by 46 per cent on the average in males and by 31.8 per cent in females. 3. Since arterial pressure was not significantly depressed it was concluded that renal vasoconstriction occurs in chronic anemia, possibly as a homeostatic device for the diversion of blood to tissues more sensitive to oxygen lack. The relatively small reduction of filtration fraction implies afferent and efferent arteriolar vasoconstriction with dominance by the afferent arterioles. These changes were shown to be reversible, a return to normal values paralleling the return of the blood picture to normal. 4. Diodrast Tm was reduced significantly in 9 of 10 patients while the values of glucose Tm were normal in 6 of 7 patients. The normal values for glucose Tm indicated continued operation of all glomeruli and implied the absence of shunting or of cessation of blood flow in any significant portion of the kidney. The fall in diodrast Tm, which appeared to be reversible in 2 of 4 individuals, was interpreted as evidence of intracellular dysfunction rather than destruction or inactivation of nephrons.

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