Renal vascular resistance in normal children - a color Doppler study

1997 ◽  
Vol 11 (2) ◽  
pp. 182-185 ◽  
Author(s):  
Ghi-Jen Lin ◽  
Tsang-Wee Cher
Keyword(s):  
Vascular Resistance ◽  
Color Doppler ◽  
Renal Vascular Resistance ◽  
Normal Children ◽  
Doppler Study ◽  
Renal Vascular

scholarly journals Determinants of Intravascular Resistance in Indian Diabetic Nephropathy Patients: A Hospital-Based Study

2011 ◽  
Vol 2011 ◽  
pp. 1-7
Author(s):  
Anubhav Thukral ◽  
Manish Mishra ◽  
Vaibhava Srivastava ◽  
Hemant Kumar ◽  
Amit Nandan Dhar Dwivedi ◽  
...  
Keyword(s):  
Diabetic Nephropathy ◽  
High Risk ◽  
Vascular Resistance ◽  
Color Doppler ◽  
Renal Vascular Resistance ◽  
Metabolic Dysregulation ◽  
Duration Of Disease ◽  
Incipient Diabetic Nephropathy ◽  
Raas Inhibitors ◽  
Renal Vascular

Aims and Objectives. Metabolic dysregulation has failed to explain clinical variability of patients with diabetic nephropathy and hence a renewed interest emerged in haemodynamic factors as determinant of progression and development of diabetic nephropathy. We therefore studied for various factors which can correlate with raised renal vascular resistance in diabetic nephropathy.Material and Methods. Renal vascular resistance was measured in patients with established and incipient diabetic nephropathy and compared with controls using noninvasive color Doppler examinations of intrarenal vasculature.Results. Renal vascular resistance correlated with age, duration of disease, GFR, serum creatinine, and stage of retinopathy. Renal vascular resistance was significantly reduced in patients on treatment with RAAS inhibitors and insulin, than those on OHA and antihypertensives other than RAAS inhibitors.Conclusion. The study implies that renal vascular resistance may help identify diabetics at high risk of developing nephropathy, and these set of patients could be candidates for RAAS inhibition and early insulin therapy even in patients without albuminuria.

Effects of endothelin ETA receptor antagonism with PD 156707 on hemodynamics and renal vascular resistance in rabbits

1997 ◽  
Vol 321 (3) ◽  
pp. 295-300 ◽  
Author(s):  
Diane P Ignasiak ◽  
Thomas B McClanahan ◽  
Lori J Saganek ◽  
Ronald E Potoczak ◽  
Hussein Hallak ◽  
...  
Keyword(s):  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Receptor Antagonism ◽  
Eta Receptor ◽  
Renal Vascular

scholarly journals Associations of renal vascular resistance with albuminuria in adolescents and young adults

2011 ◽  
Vol 26 (12) ◽  
pp. 3943-3949 ◽  
Author(s):  
C.-W. Tsai ◽  
C.-C. Kuo ◽  
C.-F. Wu ◽  
K.-L. Chien ◽  
V.-C. Wu ◽  
...  
Keyword(s):  
Young Adults ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Adolescents And Young Adults ◽  
Renal Vascular

Antenatal dexamethasone and renal vascular resistance in preterm infants

2007 ◽  
Vol 43 (4) ◽  
pp. 303-306 ◽  
Author(s):  
Norma Amador-Licona ◽  
Juan Manuel Guízar-Mendoza ◽  
Jesús Alejandro Maciel-Miranda ◽  
Gustavo Romero-Gutiérrez
Keyword(s):  
Preterm Infants ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Renal Vascular

scholarly journals Role of Renocortical Cyclooxygenase-2 for Renal Vascular Resistance and Macula Densa Control of Renin Secretion

2001 ◽  
Vol 12 (5) ◽  
pp. 867-874
Author(s):  
HAYO CASTROP ◽  
FRANK SCHWEDA ◽  
KARL SCHUMACHER ◽  
KONRAD WOLF ◽  
ARMIN KURTZ
Keyword(s):  
Vascular Resistance ◽  
Macula Densa ◽  
Renal Vascular Resistance ◽  
Renin Secretion ◽  
Expression Level ◽  
Flow Rates ◽  
Low Salt ◽  
Cox 2 ◽  
Renal Vascular

Abstract. This study aimed to assess the role of cyclooxygenase-2 (COX-2)-derived prostanoids for the macula densa control of renal afferent arteriolar resistance and for renin secretion. For this purpose, studied were the effects of blocking macula densa salt transport by the loop diuretic bumetanide (100 μM) on renal perfusate flow and on renin secretion in isolated perfused rats, in which renocortical COX-2 expression was prestimulated in vivo by treatment with the angiotensin-converting enzyme inhibitor ramipril, with low-salt diet, or with a combination of both. These maneuvers stimulated COX-2 expression in an order of ramipril + low salt ≫ low salt > ramipril > controls. Flow rates through isolated kidneys at a constant pressure of 100 mmHg were dependent on the pretreatment regimen, in the way that they went in parallel with COX-2 expression. The COX-2 inhibitor NS-398 (10 μM) lowered flow rates depending on the COX-2 expression level and was most pronounced therefore after pretreatment with low salt + ramipril. NS-398 did not change the increase of flow in response to bumetanide but attenuated the stimulation of renin secretion in response to bumetanide in a manner depending on the expression level of COX-2. These findings suggest that in states of increased renocortical expression of COX-2, overall renal vascular resistance and the macula densa control of renin secretion become dependent on COX-2—derived prostanoids.

scholarly journals Enhanced Responses of Blood Pressure, Renal Function, and Aldosterone to Angiotensin I in the DD Genotype Are Blunted by Low Sodium Intake

2002 ◽  
Vol 13 (4) ◽  
pp. 1025-1033
Author(s):  
Frank G. H. van der Kleij ◽  
Paul E. de Jong ◽  
Rob H. Henning ◽  
Dick de Zeeuw ◽  
Gerjan Navis
Keyword(s):  
Renal Function ◽  
Vascular Resistance ◽  
Sodium Intake ◽  
Renal Vascular Resistance ◽  
Hemodynamic Parameters ◽  
Angiotensin I ◽  
Low Sodium ◽  
Renal Hemodynamic ◽  
Intake Level ◽  
Renal Vascular

ABSTRACT. Angiotensin-converting enzyme (ACE) activity is increased in the DD genotype, but the functional significance for renal function is unknown. Blunted responses of BP and proteinuria to ACE inhibition among DD renal patients during periods of high sodium intake were reported. It was therefore hypothesized that sodium status affects the phenotype in the ACE I/D polymorphism. The effects of angiotensin I (AngI) and AngII among 27 healthy subjects, with both low (50 mmol sodium/d) and liberal (200 mmol sodium/d) sodium intakes, were studied. Baseline mean arterial pressure (MAP) values, renal hemodynamic parameters, and renin-angiotensin system parameters were similar for all genotypes with either sodium intake level. With liberal sodium intake, the increases in MAP, renal vascular resistance, and aldosterone levels during AngI infusion (8 ng/kg per min) were significantly higher for the DD genotype, compared with the ID and II genotypes (all parameters presented as percent changes ± 95% confidence intervals), with mean MAP increases of 22 ± 2% (DD genotype), 13 ± 5% (ID genotype), and 12 ± 6% (II genotype) (P < 0.05), mean increases in renal vascular resistance of 100.1 ± 19.7% (DD genotype), 73.0 ± 16.3% (ID genotype), and 63.2 ± 16.9% (II genotype) (P < 0.05), and increases in aldosterone levels of 650 ± 189% (DD genotype), 343 ± 71% (ID genotype), and 254 ± 99% (II genotype) (P < 0.05). Also, the decrease in GFR was more pronounced for the DD genotype, with mean decreases of 17.9 ± 4.7% (DD genotype), 8.8 ± 3.4% (ID genotype), and 6.4 ± 5.9% (II genotype) (P < 0.05). The effective renal plasma flow, plasma AngII concentration, and plasma renin activity values were similar for the genotypes. In contrast, with low sodium intake, the responses to AngI were similar for all genotypes. The responses to AngII were also similar for all genotypes, with either sodium intake level. In conclusion, the responses of MAP, renal hemodynamic parameters, and aldosterone concentrations to AngI are enhanced for the DD genotype with liberal but not low sodium intake. These results support the presence of gene-environment interactions between ACE genotypes and dietary sodium intake.

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