scholarly journals Blockade of renal medullary bradykinin B2 receptors increases tubular sodium reabsorption in rats fed a normal-salt diet

2008 ◽  
Vol 295 (3) ◽  
pp. F811-F817 ◽  
Author(s):  
Sema-Hayriye Sivritas ◽  
David W. Ploth ◽  
Wayne R. Fitzgibbon
Keyword(s):  
Blood Flow ◽  
Left Kidney ◽  
Treated Group ◽  
Control Group ◽  
Sodium Reabsorption ◽  
Salt Diet ◽  
Excretory Function ◽  
Time Control ◽  
Medullary Blood Flow ◽  
Hoe 140

The present study was performed to test the hypothesis that under normal physiological conditions and/or during augmentation of kinin levels, intrarenal kinins act on medullary bradykinin B2 (BKB2) receptors to acutely increase papillary blood flow (PBF) and therefore Na+ excretion. We determined the effect of acute inner medullary interstitial (IMI) BKB2 receptor blockade on renal hemodynamics and excretory function in rats fed either a normal (0.23%)- or a low (0.08%)-NaCl diet. For each NaCl diet, two groups of rats were studied. Baseline renal hemodynamic and excretory function were determined during IMI infusion of 0.9% NaCl into the left kidney. The infusion was then either changed to HOE-140 (100 μg·kg−1·h−1, treated group) or maintained with 0.9% NaCl (time control group), and the parameters were again determined. In rats fed a normal-salt diet, HOE-140 infusion decreased left kidney Na+ excretion (urinary Na+ extraction rate) and fractional Na+ excretion by 40 ± 5% and 40 ± 4%, respectively ( P < 0.01), but did not alter glomerular filtration rate, inner medullary blood flow (PBF), or cortical blood flow. In rats fed a low-salt diet, HOE-140 infusion did not alter renal regional hemodynamics or excretory function. We conclude that in rats fed a normal-salt diet, kinins act tonically via medullary BKB2 receptors to increase Na+ excretion independent of changes in inner medullary blood flow.

Hypothermic Circulatory Arrest: Renal Protection by Atrial Natriuretic Peptide

2009 ◽  
Vol 17 (4) ◽  
pp. 401-407 ◽  
Author(s):  
Masahiro Ohno ◽  
Tadashi Omoto ◽  
Masaomi Fukuzumi ◽  
Masaya Oi ◽  
Noboru Ishikawa ◽  
...  
Keyword(s):  
Blood Flow ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Circulatory Arrest ◽  
Treated Group ◽  
Hypothermic Circulatory Arrest ◽  
Control Group ◽  
Myeloperoxidase Activity ◽  
Medullary Blood Flow ◽  
Atrial Natriuretic

Moderate hypothermic circulatory arrest with selective cerebral perfusion has been developed for cerebral protection during thoracic aortic surgery. However, visceral organs, particularly the kidneys, suffer greater tissue damage under moderate hypothermic circulatory arrest, and acute renal failure after hypothermic circulatory arrest is an independent risk factor for early and late mortality. This study investigated whether atrial natriuretic peptide could prevent the reduction in renal perfusion and protect renal function after moderate hypothermic circulatory arrest. Twelve pigs cooled to 30°C during cardiopulmonary bypass were randomly assigned to a peptide-treated group of 6 and a control group of 6. Moderate hypothermic circulatory arrest was induced for 60 min. Systemic arterial mean pressure and renal artery flow did not differ between groups during the study. However, renal medullary blood flow increased significantly in the peptide-treated group after hypothermic circulatory arrest. Myeloperoxidase activity was significantly reduced in the medulla of the peptide-treated group. Renal medullary ischemia after hypothermic circulatory arrest was ameliorated by atrial natriuretic peptide which increased medullary blood flow and reduced sodium reabsorption in the medulla. Atrial natriuretic peptide also reduced the release of an inflammatory marker after ischemia in renal tissue.

Influence of the renal medullary circulation on the control of sodium excretion

1993 ◽  
Vol 265 (5) ◽  
pp. R963-R973 ◽  
Author(s):  
R. J. Roman ◽  
A. P. Zou
Keyword(s):  
Blood Flow ◽  
Renal Perfusion ◽  
Sodium Reabsorption ◽  
Doppler Flowmetry ◽  
Medullary Blood Flow ◽  
Tubular Sodium Reabsorption ◽  
Vasa Recta ◽  
Urinary Concentrating Ability ◽  
Reliable Methods

Although the role of the renal medullary circulation in the control of urinary concentrating ability is well established, its potential influence on tubular sodium reabsorption is not generally recognized. Nearly 30 years ago, changes in the intrarenal distribution of blood flow were first proposed to contribute to the natriuretic response to volume expansion. However, the lack of reliable methods for studying medullary blood flow limited progress in this area. The recent development of laser-Doppler flowmetry and videomicroscopic techniques for the study of the vasa recta circulation has renewed interest in the role of medullary hemodynamics in the control of sodium reabsorption. Results of these studies indicate that changes in renal medullary hemodynamics alter renal interstitial pressure and the medullary solute gradient and play an important role in the natriuretic response to elevations in renal perfusion pressure, intravenous infusion of saline, and changes in tubular sodium reabsorption produced by vasoactive compounds. What is emerging from these studies is the view that changes in renal medullary hemodynamics represent an important but misunderstood and long-ignored factor in the control of tubular sodium reabsorption.

Effect of chemical sympathectomy on cerebral blood flow in rats

1991 ◽  
Vol 75 (6) ◽  
pp. 906-910 ◽  
Author(s):  
Hidenori Kobayashi ◽  
Minoru Hayashi ◽  
Hirokazu Kawano ◽  
Yuji Handa ◽  
Masanori Kabuto ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Systemic Blood Pressure ◽  
Treated Group ◽  
Control Group ◽  
Electron Microscopic ◽  
Content Type ◽  
Left Lateral Ventricle ◽  
6 Hydroxydopamine ◽  
Fine Print

✓ Thirty male Wistar rats, weighing 350 to 400 gm each, received stereotactic injections of 6-hydroxydopamine (300 µg/kg) into the left lateral ventricle. The same amount of saline was injected into a control group of 15 rats. Seven days after this procedure, cerebral blood flow (CBF) was measured by the hydrogen clearance method. A hypertensive condition at a mean arterial pressure of about 160 mm Hg was maintained for 1 hour by intravenous infusion of phenylephrine. In the 6-hydroxydopamine-treated group, CBF increased significantly after the elevation of systemic blood pressure compared with that in the control group, and cerebral autoregulation was impaired. After a 1-hour study, the specific gravity of the cerebral tissue in the treated group significantly decreased; electron microscopic studies at that time revealed brain edema. It is suggested that depletion of brain noradrenaline levels causes a disturbance in cerebral microvascular tone and renders the cerebral blood vessels more vulnerable to hypertension.

Abstract P166: The Effects of V2 Receptor Antagonist Treatment on the Renal Medullary Circulation and Urinary Sodium Excretion in Rat

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Yusuke Ohsaki ◽  
Takefumi Mori ◽  
Kento Akao ◽  
Yoshimi Nakamichi ◽  
Chika Takahashi ◽  
...  
Keyword(s):  
Blood Flow ◽  
Urine Volume ◽  
Urinary Sodium Excretion ◽  
Urinary Sodium ◽  
Sodium Reabsorption ◽  
No Production ◽  
Doppler Flowmetry ◽  
Medullary Blood Flow ◽  
V2 Receptor ◽  
Renal Medullary Blood Flow

Objective: V2 receptor (V2R) antagonist increases aquaresis, and was reported to have renoprotective and natriuretic effect, although the mechanism is not fully clarified. Renal medullary hemodynamics contributes sodium retention and renal injury. Therefore, the present study was designed to evaluate the effect of V2R antagonist on renal medullary blood flow. Methods: Catheter was inserted in femoral artery and vein of anesthetized SD rats to monitor blood pressure (BP), heart rate (HR) and to infuse drugs, respectively. Renal medullary blood flow (MBF) and renal medullary oxygen pressure (pO2) were measured with laser-Doppler flowmetry or oxygen microelectrode, respectively. V2R antagonist, OPC-31260 (OPC, 0.25mg/kg bw/h) or furosemide (Furo, 0.5mg/kg bw/h) was intravenously administrated for 90min. Urine was collected in 30 min interval and urinary sodium (UNaV), hydrogen peroxide (UH2O2V) and [nitrate + nitrite] (UNOxV) excretion were measured. Results: OPC and Furo treatment did not change BP and HR. Urine volume was significantly increased by OPC (1.1+0.2 to 6.1+0.5 g/30 min) and Furo (1.4+0.6 to 4.7+0.3 g/30 min) treatment but was not different between groups. MBF was significantly decreased in Furo (12+4% decrease from baseline), while OPC did not changed MBF (1+3% increase from baseline). pO2 was significantly increased by both OPC and Furo treatment (20+6 and 27+10% increase from baseline, respectively). UNaV was significantly increased in OPC (0.10+0.02 to 0.44+0.05 mEq/30 min) and Furo (0.14+0.08 to 0.69+0.06 mEq/30 min) treatment, the increase of UNaV was significantly higher in Furo than OPC group. UH2O2V was significantly increased by Furo treatment (16+4 to 28+6 nmol/30 min), while did not change in OPC treatment (10+2 to 19+4 nmol/30 min). UNOx was significantly increased in OPC treatment (211+30 to 376+45 nmol/30 min), while did not change in Furo treatment (142+27 to 237+75 nmol/30 min). Conclusion: OPC treatment increased NO production. Increased NO could contribute to decrease of sodium reabsorption, result in increase of renal medullary pO2. This scheme could be one on the mechanisms of renal protective effect by V2R antagonist treatment.

Noninvasive measurement of intrarenal blood flow distribution: kinetic model of renal 123I-hippuran handling

1995 ◽  
Vol 269 (4) ◽  
pp. F571-F580 ◽  
Author(s):  
W. M. Janssen ◽  
H. Beekhuis ◽  
R. de Bruin ◽  
P. E. de Jong ◽  
D. de Zeeuw
Keyword(s):  
Blood Flow ◽  
Kinetic Model ◽  
Atrial Natriuretic Factor ◽  
Left Kidney ◽  
Flow Distribution ◽  
Noninvasive Measurement ◽  
Blood Flow Distribution ◽  
Angiotensin I ◽  
Medullary Blood Flow ◽  
Intrarenal Blood Flow

A new technique for noninvasive measurement of intrarenal blood flow distribution over cortex and medulla is proposed. The technique involves analysis of 123I-labeled hippuran renography, according to a kinetic model that describes the flow of 123I-hippuran from the heart (input) through the renal cortex and medulla to the bladder (output). The method is validated and compared with the standard microsphere injection technique in anesthetized dogs. Changes in intrarenal blood flow distribution were induced by infusion of placebo (n = 6), angiotensin I (n = 5), or atrial natriuretic factor (n = 5). Baseline percentage medullary blood flow in the left kidney was 12 +/- 1% of total renal blood flow measured with microspheres and 15 +/- 1% with renography. During infusion of the placebo, medullary blood flow decreased slightly compared with baseline, as measured with both methods, by 2 +/- 6 (microspheres) and 1 +/- 8% (renography). Infusion of angiotensin I caused a marked fall in medullary blood flow by 42 +/- 11 (microspheres) and 57 +/- 8% (renography). In contrast, infusion of atrial natriuretic factor caused a small rise in medullary blood flow as measured with both methods (9 +/- 3 and 12 +/- 11%, respectively). The absolute and percent changes in medullary blood flow measured with renography correlated with those measured with microspheres (left kidney: r = 0.67, P = 0.005; r = 0.71, P = 0.003, respectively; right kidney: r = 0.62, P = 0.01; r = 0.68, P = 0.004, respectively). We conclude that the proposed kinetic model of renal 123I-hippuran handling can be used to measure changes in intrarenal blood flow distribution and, because of its noninvasive character, may be of use in clinical studies.

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.

Angiotensin II and renal medullary blood flow in Lyon rats

2003 ◽  
Vol 284 (2) ◽  
pp. F365-F372 ◽  
Author(s):  
Albert Sarkis ◽  
Kiao Ling Liu ◽  
Ming Lo ◽  
Daniel Benzoni
Keyword(s):  
Blood Flow ◽  
Receptor Blockade ◽  
Ang Ii ◽  
Acute Effects ◽  
Medullary Blood Flow ◽  
Low Blood Pressure ◽  
Renal Medullary Blood Flow ◽  
Hoe 140 ◽  
High Doses ◽  
Dose Dependent

The present study evaluated the acute effects of ANG II (5–480 ng/kg iv) and phenylephrine (PE; 0.2–146 μg/kg iv) on total renal (RBF) and medullary blood flow (MBF) in anesthetized Lyon hypertensive (LH) and low-blood-pressure (LL) rats. ANG II and PE induced dose-dependent decreases in both RBF and MBF, which were greater in LH than in LL rats. Interestingly, after ANG II, but not after PE, the initial medullary vasoconstriction was followed by a long-lasting and dose-dependent vasodilation that was significantly blunted in LH compared with LL rats. The mechanisms of the MBF effects of ANG II were studied in LL rats only. Blockade of AT1 receptors with losartan (10 mg/kg) abolished all the effects of ANG II, whereas AT2 receptor blockade with PD-123319 (50 μg · kg−1 · min−1iv) did not change these effects. Indomethacin (5 mg/kg) decreased by ∼90% the medullary vasodilation induced by the lowest doses of ANG II (from 15 ng/kg). In contrast, N G-nitro-l-arginine methyl ester (10 mg/kg and 0.1 mg · kg−1 · min−1iv) and the bradykinin B2-receptor antagonist HOE-140 (20 μg/kg and 10 μg · kg−1 · min−1iv) markedly lowered the medullary vasodilation at the highest doses of ANG II only. In conclusion, this study shows that LH rats exhibit an altered MBF response to ANG II compared with LL rats and indicates that the AT1 receptor-mediated medullary vasodilator response to low doses of ANG II is mainly due to the release of PGs, whereas the dilator response to high doses of ANG II has additional nitric oxide- and kinin-dependent components.

scholarly journals Bradykinin Antagonist Counteracts the Acute Effect of Both Angiotensin-Converting Enzyme Inhibition and of Angiotensin Receptor Blockade on the Lower Limit of Autoregulation of Cerebral Blood Flow

2013 ◽  
Vol 34 (3) ◽  
pp. 467-471 ◽  
Author(s):  
Sigurdur T Sigurdsson ◽  
Olaf B Paulson ◽  
Arne Høj Nielsen ◽  
Svend Strandgaard
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Angiotensin Converting Enzyme ◽  
Lower Limit ◽  
Ace Inhibitor ◽  
Control Group ◽  
Converting Enzyme ◽  
Angiotensin Receptor ◽  
Bradykinin Antagonist ◽  
Hoe 140

The lower limit of autoregulation of cerebral blood flow (CBF) can be modulated with both angiotensin-converting enzyme (ACE) inhibitors and angiotensin receptor blockers (ARB). The influence of bradykinin antagonism on ARB-induced changes was the subject of this study. CBF was measured in Sprague–Dawley rats with laser Doppler technique. The blood pressure was lowered by controlled bleeding. Six groups of rats were studied: a control group and five groups given drugs intravenously: an ACE inhibitor (enalaprilat), an ARB (candesartan), a bradykinin-2 receptor antagonist (Hoe 140), a combination of enalaprilat and Hoe 140, and a combination of candesartan and Hoe 140. In the control group, the lower limit of CBF autoregulation was 54±9 mm Hg (mean±s.d.), with enalaprilat it was 46±6, with candesartan 39±8, with Hoe 140 53±6, with enalaprilat/Hoe 140 52±6, and with candesartan/Hoe 140 50±7. Both enalaprilat and candesartan lowered the lower limit of autoregulation of CBF significantly. The bradykinin antagonist abolished not only the effect of the ACE inhibitor but surprisingly also the effect of the ARB on the lower limit of CBF autoregulation, the latter suggesting an effect on intravascular bradykinin.

Effect of mesangiolysis on autoregulation of renal blood flow and glomerular filtration rate in rats

1992 ◽  
Vol 262 (3) ◽  
pp. F361-F366 ◽  
Author(s):  
B. M. Iversen ◽  
F. I. Kvam ◽  
K. Matre ◽  
L. Morkrid ◽  
G. Horvei ◽  
...  
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Mesangial Cells ◽  
Control Volume ◽  
Left Kidney ◽  
Control Group

Interlobular arteries and afferent arterioles are involved in autoregulation of renal blood flow (RBF) and glomerular filtration rate (GFR). The question of whether the contractile mesangial cells are also involved in autoregulation was investigated in Wistar rats. Autoregulation of RBF was examined before and 1 h after infusion of antithymocyte (anti-Thy 1-1) antibodies, and both RBF and GFR autoregulation were examined 30 h after the infusion of antibodies. Mesangial cell destruction was present 30 h after the infusion of antibodies. The angiotensin II-induced contraction of isolated glomeruli (70% of control volume, P less than 0.001) was abolished after the glomeruli had been exposed to anti-Thy 1-1 in vitro. RBF, as well as the lower limit of RBF autoregulation, were not different from control 30 h after the infusion (82 +/- 5 vs. 79 +/- 4 mmHg, P greater than 0.10). Autoregulation of GFR was maintained in the control group but was restricted in the experimental group (autoregulatory index: 0.71 +/- 0.42 for left kidney, 0.02 +/- 0.35 for control; P less than 0.05). The afferent arteriolar diameter was unchanged 30 h after the infusion of antibodies (17.8 +/- 0.8 vs. 17.6 +/- 0.4 microns, P greater than 0.10). One hour after infusion of the antibodies, RBF autoregulation was normal. It is concluded that mesangial cells do not seem to be involved in RBF autoregulation, but may in part influence autoregulation of GFR during pressure reduction.

Effect of α-adrenergic blockade on the cerebrovascular response to increased intracranial pressure after hemorrhage

1998 ◽  
Vol 89 (3) ◽  
pp. 454-459 ◽  
Author(s):  
Ingunn R. Rise ◽  
Ole J. Kirkeby
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Intracranial Pressure ◽  
Blood Loss ◽  
Treated Group ◽  
Control Group ◽  
Adrenergic Blockade ◽  
Content Type ◽  
Cerebrovascular Resistance ◽  
Fine Print

Object. In this study the authors tested the hypothesis that hemorrhagic hypotension and high intracranial pressure induce an increase in cerebrovascular resistance that is caused by sympathetic compensatory mechanisms and can be modified by α-adrenergic blockade. Methods. Continuous measurements of cerebral blood flow were obtained using laser Doppler microprobes placed in the cerebral cortex in anesthetized pigs during induced hemorrhagic hypotension and high cerebrospinal fluid pressure. Eight pigs received 2 mg/kg phentolamine in 10 ml saline, and 13 pigs served as control animals. During high intracranial pressure occurring after blood loss, cerebral perfusion pressure (CPP) (p < 0.01) and cerebral blood flow (p < 0.01) decreased in both groups. Cerebrovascular resistance increased (p < 0.05) in the control group and decreased < 0.005) in the phentolamine-treated group. The cerebrovascular resistance was significantly lower in the phentolamine-treated group (p < 0.05) than in the control group. Cerebrovascular resistance increased at lower CPPs in the control group (linear correlation, r = 0.39, p < 0.01) and decreased with decreasing CPP in the phentolamine-treated group (linear correlation, r = 0.76, p < 0.001). Conclusions. This study shows that the deleterious effects on cerebral hemodynamics induced by blood loss in combination with high intracranial pressure are inhibited by α-adrenergic blockade. This suggests that these responses are caused by α-adrenergically mediated cerebral vasoconstriction.

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