scholarly journals CMR 2007: 6.03: Contrast-enhanced destruction–replenishment CPS ultrasound for quantifying cortical and medullary blood flow in a rat kidney model

2007 ◽  
Vol 2 (6) ◽  
pp. 287-287
Author(s):  
R. Pollard ◽  
M. Tartis ◽  
J. Stern ◽  
S. E. Bennett ◽  
K. Ferrara
Keyword(s):  
Blood Flow ◽  
Rat Kidney ◽  
Medullary Blood Flow ◽  
Contrast Enhanced

Nitric oxide modulates angiotensin II- and norepinephrine-dependent vasoconstriction in rat kidney

1996 ◽  
Vol 270 (3) ◽  
pp. R630-R635 ◽  
Author(s):  
N. Parekh ◽  
L. Dobrowolski ◽  
A. P. Zou ◽  
M. Steinhausen
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Rat Kidney ◽  
Ang Ii ◽  
No Donor ◽  
Renal Vasoconstriction ◽  
Medullary Blood Flow ◽  
Series Of Experiments ◽  
Synthase Inhibitor

This study compared the vasoconstrictor action of angiotensin II (ANG II) and norepinephrine (NE) with different levels of nitric oxide (NO) in the kidney of anesthetized rats. In one series of experiments, the drugs were infused intravenously, and systemic NO content was reduced by a NO synthase inhibitor, nitro-L-arginine methyl ester (L-NAME). L-NAME significantly enhanced the renal blood flow (RBF) reduction produced by ANG II from 26 to 49%, but it had no significant effect on the change in RBF induced by NE. Medullary blood flow was not influenced by either ANG II or NE given alone or given after L-NAME. In the second series of experiments, all drugs were infused into the renal artery to avoid their systemic and, hence, extrarenal effects. In these experiments, renal content of NO was increased by the NO donor sodium nitroprusside (SNP), decreased by L-NAME, or restored by replacing endogenous NO by exogenous NO (L-NAME + SNP). Effects of both ANG II and NE on RBF were similarly and significantly attenuated by SNP (60% of control), enhanced by L-NAME (200% of control), and restored by L-NAME + SNP (90% of control, not significant). Our results indicate that NO attenuates the renal vasoconstriction due to ANG II or NE and that the antagonism between vasoconstrictors and NO is not due to a constrictor-induced production of NO because exogenous and endogenous NO were equally effective.

scholarly journals Effects of pH and medullary blood flow on oxygen transport and sodium reabsorption in the rat outer medulla

2010 ◽  
Vol 298 (6) ◽  
pp. F1369-F1383 ◽  
Author(s):  
Jing Chen ◽  
Aurélie Edwards ◽  
Anita T. Layton
Keyword(s):  
Blood Flow ◽  
Rat Kidney ◽  
Sodium Reabsorption ◽  
Vascular Bundles ◽  
Outer Medulla ◽  
Medullary Blood Flow ◽  
Blood Ph ◽  
Effects Of Ph ◽  
Tubular Flow

We used a mathematical model of O2 transport and the urine concentrating mechanism of the outer medulla of the rat kidney to study the effects of blood pH and medullary blood flow on O2 availability and Na+ reabsorption. The model predicts that in vivo paracellular Na+ fluxes across medullary thick ascending limbs (mTALs) are small relative to transcellular Na+ fluxes and that paracellular fluxes favor Na+ reabsorption from the lumen along most of the mTAL segments. In addition, model results suggest that blood pH has a significant impact on O2 transport and Na+ reabsorption owing to the Bohr effect, according to which a lower pH reduces the binding affinity of hemoglobin for O2. Thus our model predicts that the presumed greater acidity of blood in the interbundle regions, where mTALs are located, relative to that in the vascular bundles, facilitates the delivery of O2 to support the high metabolic requirements of the mTALs and raises the concentrating capability of the outer medulla. Model results also suggest that increases in vascular and tubular flow rates result in disproportional, smaller increases in active O2 consumption and mTAL active Na+ transport, despite the higher delivery of O2 and Na+. That is, at a sufficiently high medullary O2 supply, O2 demand in the outer medulla does not adjust precisely to changes in O2 delivery.

scholarly journals Effects of contrast media and mannitol on renal medullary blood flow and red cell aggregation in the rat kidney

1996 ◽  
Vol 49 (5) ◽  
pp. 1268-1275 ◽  
Author(s):  
Per Liss ◽  
Anders Nygren ◽  
Ulf Olsson ◽  
Hans R. Ulfendahl ◽  
Uno Erikson
Keyword(s):  
Blood Flow ◽  
Contrast Media ◽  
Rat Kidney ◽  
Cell Aggregation ◽  
Red Cell ◽  
Medullary Blood Flow ◽  
Renal Medullary Blood Flow ◽  
Red Cell Aggregation

Acute effect of cyclosporin on inner medullary blood flow in normal and postischemic rat kidney

1990 ◽  
Vol 258 (5) ◽  
pp. F1139-F1144
Author(s):  
Y. Yagil
Keyword(s):  
Blood Flow ◽  
Rat Kidney ◽  
Electromagnetic Flowmeter ◽  
Renal Medulla ◽  
Acute Effect ◽  
Acute Administration ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Group 2 ◽  
Group 1

Acute cyclosporin A (CysA) nephrotoxicity has been attributed to intrarenal vasoconstriction. It has been previously demonstrated that CysA decreases whole kidney and cortical blood flow. The effect of CysA on medullary blood flow has not been adequately studied, despite the high susceptibility of structures in the renal medulla to ischemia and the common use of CysA after the kidney is subjected to transient ischemia. To determine its effects on medullary blood flow in the normal and postischemic kidney, CysA was administered acutely in anesthetized Munich-Wistar rats at doses ranging from 4 to 20 mg/kg. Total renal blood flow (TRBF) and glomerular filtration rate (GFR) were determined in normal kidneys (group 1) by standard clearance techniques before and after infusion of CysA. In animals subjected to 40-min unilateral renal ischemia (group 2) TRBF was measured with an electromagnetic flowmeter. Vasa recta blood flow was determined in both groups by fluorescence videomicroscopy. In group 1, infusion with 20 mg/kg CysA, but not with 4 or 8 mg/kg, increased renal vascular resistance (RVR) and decreased TRBF. GFR was not affected and filtration fraction increased. Vasa recta blood flow was not significantly altered. In group 2, 20 mg/kg CysA increased RVR and decreased TRBF. Vasa recta blood flow decreased significantly in the descending but not in the ascending vasa recta. These results suggest that, in the normal kidney, vasa recta blood flow in the renal medulla is not affected by acute administration of CysA, whereas in the postischemic kidney, CysA decreases blood flow preferentially in the descending vasa recta, in proportion to the decline in TRBF.

Glucagon increases medullary interstitial electrolyte concentration in rat kidney

1995 ◽  
Vol 73 (9) ◽  
pp. 1289-1291 ◽  
Author(s):  
E. Kompanowska-Jezierska ◽  
J. Sadowski ◽  
A. Walkowska
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Rat Kidney ◽  
Urine Concentration ◽  
Ion Concentration ◽  
High Dose ◽  
Nacl Transport ◽  
Medullary Blood Flow

In anesthetized rats, tissue electrical admittance of the inner medulla (a measure of total ion concentration in the interstitium), medullary blood flow (laser Doppler technique), and renal clearances were measured simultaneously before and during i.v. infusion of glucagon at 110 and 330 ng∙min−1∙kg−1 body weight. Admittance increased modestly, 5.4% after a large glucagon dose (p < 0.01), whereas medullary blood flow was stable. Glomerular filtration rate increased transiently and then fell during high-dose glucagon infusion. The increase in tissue electrolyte (mostly NaCl) concentration in the medulla observed with stable medullary blood flow and decreasing glomerular filtration rate indicates that stimulation of NaCl reabsorption in the medullary ascending limb of Henle's loop by glucagon was the mechanism underlying augmentation of medullary ionic hypertonicity. This suggests that glucagon can contribute to the urine concentration process.Key words: glucagon, loop of Henle, tubular NaCl transport, medullary blood flow.

Role of renal medullary adenosine in the control of blood flow and sodium excretion

1999 ◽  
Vol 276 (3) ◽  
pp. R790-R798 ◽  
Author(s):  
Ai-Ping Zou ◽  
Kasem Nithipatikom ◽  
Pin-Lan Li ◽  
Allen W. Cowley
Keyword(s):  
Blood Flow ◽  
Sodium Excretion ◽  
Renal Medulla ◽  
Urine Flow ◽  
Doppler Flowmetry ◽  
Blood Flows ◽  
Medullary Blood Flow ◽  
Adenosine Concentration ◽  
Interstitial Infusion

This study determined the levels of adenosine in the renal medullary interstitium using microdialysis and fluorescence HPLC techniques and examined the role of endogenous adenosine in the control of medullary blood flow and sodium excretion by infusing the specific adenosine receptor antagonists or agonists into the renal medulla of anesthetized Sprague-Dawley rats. Renal cortical and medullary blood flows were measured using laser-Doppler flowmetry. Analysis of microdialyzed samples showed that the adenosine concentration in the renal medullary interstitial dialysate averaged 212 ± 5.2 nM, which was significantly higher than 55.6 ± 5.3 nM in the renal cortex ( n = 9). Renal medullary interstitial infusion of a selective A1antagonist, 8-cyclopentyl-1,3-dipropylxanthine (DPCPX; 300 pmol ⋅ kg−1 ⋅ min−1, n = 8), did not alter renal blood flows, but increased urine flow by 37% and sodium excretion by 42%. In contrast, renal medullary infusion of the selective A2 receptor blocker 3,7-dimethyl-1-propargylxanthine (DMPX; 150 pmol ⋅ kg−1 ⋅ min−1, n = 9) decreased outer medullary blood flow (OMBF) by 28%, inner medullary blood flows (IMBF) by 21%, and sodium excretion by 35%. Renal medullary interstitial infusion of adenosine produced a dose-dependent increase in OMBF, IMBF, urine flow, and sodium excretion at doses from 3 to 300 pmol ⋅ kg−1 ⋅ min−1( n = 7). These effects of adenosine were markedly attenuated by the pretreatment of DMPX, but unaltered by DPCPX. Infusion of a selective A3receptor agonist, N 6-benzyl-5′-( N-ethylcarbonxamido)adenosine (300 pmol ⋅ kg−1 ⋅ min−1, n = 6) into the renal medulla had no effect on medullary blood flows or renal function. Glomerular filtration rate and arterial pressure were not changed by medullary infusion of any drugs. Our results indicate that endogenous medullary adenosine at physiological concentrations serves to dilate medullary vessels via A2 receptors, resulting in a natriuretic response that overrides the tubular A1 receptor-mediated antinatriuretic effects.

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