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 Impact of nitric oxide-mediated vasodilation on outer medullary NaCl transport and oxygenation

2012 ◽  
Vol 303 (7) ◽  
pp. F907-F917 ◽  
Author(s):  
Aurélie Edwards ◽  
Anita T. Layton
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Supply And Demand ◽  
Vascular Bundles ◽  
Concentration Gradients ◽  
Outer Medulla ◽  
Nacl Transport ◽  
Reciprocal Interactions ◽  
Medullary Blood Flow ◽  
Vasa Recta

The present study aimed to elucidate the reciprocal interactions between oxygen (O2), nitric oxide (NO), and superoxide (O2−) and their effects on vascular and tubular function in the outer medulla. We expanded our region-based model of transport in the rat outer medulla (Edwards A, Layton AT. Am J Physiol Renal Physiol 301: F979–F996, 2011) to incorporate the effects of NO on descending vasa recta (DVR) diameter and blood flow. Our model predicts that the segregation of long DVR in the center of vascular bundles, away from tubular segments, gives rise to large radial NO concentration gradients that in turn result in differential regulation of vasoactivity in short and long DVR. The relative isolation of long DVR shields them from changes in the rate of NaCl reabsorption, and hence from changes in O2 requirements, by medullary thick ascending limbs (mTALs), thereby preserving O2 delivery to the inner medulla. The model also predicts that O2− can sufficiently decrease the bioavailability of NO in the interbundle region to affect the diameter of short DVR, suggesting that the experimentally observed effects of O2− on medullary blood flow may be at least partly mediated by NO. In addition, our results indicate that the tubulovascular cross talk of NO, that is, the diffusion of NO produced by mTAL epithelia toward adjacent DVR, helps to maintain blood flow and O2 supply to the interbundle region even under basal conditions. NO also acts to preserve local O2 availability by inhibiting the rate of active Na+ transport, thereby reducing the O2 requirements of mTALs. The dual regulation by NO of oxygen supply and demand is predicted to significantly attenuate the hypoxic effects of angiotensin II.

Interactions between ADH and prostaglandins in isolated erythrocyte-perfused rat kidney

1987 ◽  
Vol 252 (2) ◽  
pp. F331-F337 ◽  
Author(s):  
W. Lieberthal ◽  
M. L. Vasilevsky ◽  
C. R. Valeri ◽  
N. G. Levinsky
Keyword(s):  
Sodium Excretion ◽  
Rat Kidney ◽  
Urine Osmolality ◽  
Sodium Reabsorption ◽  
Urinary Osmolality ◽  
Hemodynamic Characteristics ◽  
Urinary Concentrating Ability ◽  
Tubular Morphology ◽  
Isolated Kidneys

Interactions between antidiuretic hormone (ADH) and renal prostaglandins in the regulation of sodium reabsorption and urinary concentrating ability were studied in isolated erythrocyte-perfused rat kidneys (IEPK). In this model, hemodynamic characteristics are comparable to those found in vivo, and tubular morphology is preserved throughout the period of perfusion. [Deamino]-D-arginine vasopressin (dDAVP) markedly reduced fractional sodium excretion (FE Na) in the IEPK from 3.5 +/- 0.6 to 0.45 +/- 0.14%. After indomethacin, FE Na fell still further to 0.08 +/- 0.02%. In the absence of dDAVP indomethacin had no effect on sodium excretion; FE Na was 2.4 +/- 0.6% in control and 2.0 +/- 0.4% in indomethacin-treated groups. dDAVP increased urine osmolality in the IEPK to 741 +/- 26 mosmol/kg. When prostaglandin synthesis was blocked with indomethacin, urinary osmolality increased further to 1,180 +/- 94 mosmol/kg. In isolated kidneys perfused without erythrocytes (IPK), dDAVP decreased FENa from 14.5 +/- 1.8% to 9.6 +/- 1.2%; addition of indomethacin had no further effect. dDAVP increased urine osmolality only modestly to 350 +/- 12 mosmol/kg in the IPK and indomethacin did not increase concentrating ability further (342 +/- 7 mosmol/kg). Thus the IEPK (unlike the IPK) can excrete a markedly hypertonic urine in response to ADH. ADH also enhances tubular reabsorption of sodium in the IEPK. Prostaglandins inhibit both these actions of ADH but do not directly affect sodium excretion in the absence of the hormone.

Localization and regulation of the rat renal Na(+)-K(+)-2Cl- cotransporter, BSC-1

1996 ◽  
Vol 271 (3) ◽  
pp. F619-F628 ◽  
Author(s):  
C. A. Ecelbarger ◽  
J. Terris ◽  
J. R. Hoyer ◽  
S. Nielsen ◽  
J. B. Wade ◽  
...  
Keyword(s):  
Rat Kidney ◽  
Rat Colon ◽  
Thick Ascending Limb ◽  
Outer Medulla ◽  
Water Excretion ◽  
Saline Loading ◽  
Cloned Cdna ◽  
Urinary Concentrating Ability

To investigate the role of the thick ascending limb (TAL) Na(+)-K(+)-2Cl- cotransporter in regulation of water excretion, we have prepared a peptide-derived polyclonal antibody based on the cloned cDNA sequence of the rat type 1 bumetanide-sensitive cotransporter, BSC-1 (also termed "NKCC-2"). Immunoblots revealed a single broad 161-kDa band in membrane fractions of rat renal outer medulla and cortex but not from rat colon or parotid gland. A similar protein was labeled in mouse kidney. Immunoperoxidase immunohistochemistry in rat kidney revealed labeling restricted to the medullary and cortical TAL segments. Because long-term regulation of urinary concentrating ability may depend on regulation of Na(+)-K(+)-2Cl- cotransporter abundance, we used immunoblotting to evaluate the effects of several in vivo factors on expression levels of BSC-1 protein in rat kidney outer medulla. Chronic oral saline loading with 0.16 M NaCl markedly increased BSC-1 abundance. However, long-term vasopressin infusion or thirsting of rats did not affect BSC-1 abundance. Chronic furosemide infusion caused a 9-kDa upward shift in apparent molecular mass and an apparent increase in expression level. These results support the previous identification of BSC-1 as the TAL Na(+)-K(+)-2Cl- transporter and demonstrate that the expression of this transporter is regulated.

Continuous measurement of tissue blood flow by laser-Doppler spectroscopy

1977 ◽  
Vol 232 (4) ◽  
pp. H441-H448 ◽  
Author(s):  
M. D. Stern ◽  
D. L. Lappe ◽  
P. D. Bowen ◽  
J. E. Chimosky ◽  
G. A. Holloway ◽  
...  
Keyword(s):  
Blood Flow ◽  
Line Width ◽  
Rat Kidney ◽  
Tissue Perfusion ◽  
Laser Doppler ◽  
Renal Physiology ◽  
Tissue Blood Flow ◽  
Outer Cortex ◽  
Promising Tool

Laser light scattered from tissue in vivo is broadened in line width as a result of the Doppler shift produced by moving red cells in the microcirculation. A feasibility study was carried out to demonstrate use of this effect to measure and monitor tissue blood flow. Light from a helium-neon laser illuminated a 1-mm area of tissue (human skin or rat renal cortex), and the backscattered light was detected with a photomultiplier. The spectrum of the Doppler beat notes was analyzed directly with a digital spectrum analyzer, or processed by analog circuitry to yield a flow parameter based on the root-mean-square Doppler line width. This parameter was compared with 133Xe washout in the skin of volunteers subjected to UV-induced erythema and the skin of volunteers subjected to UV-induced erythema and was found to vary in an approximately linear manner with skin blood flow. The laser instrument provided continuous monitoring of blood flow fluctuations, including the pulsatile component. The instrument was used to monitor flow in the outer cortex of the rat kidney during administration of norepinephrine, angiotensin, hydralazine, dextran, dopamine, nitroprusside, and angiotensin blocked by saralasin. Dynamic and steady-state responses were consistent with known pharmacology and renal physiology, and with the assumption that vasoconstrictor angiotensin II receptors in the kidney are accessible to blood-borne inhibitors. The laser-Doppler method is a promising tool for rapid monitoring of dynamic changes in tissue perfusion.

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.

Renal medullary blood flow: its measurement and physiology

1986 ◽  
Vol 64 (7) ◽  
pp. 873-880 ◽  
Author(s):  
W. A. Cupples
Keyword(s):  
Blood Flow ◽  
Renal Medulla ◽  
Vascular Bundles ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Countercurrent Exchange ◽  
Renal Medullary Blood Flow ◽  
Urinary Concentrating Ability ◽  
Velocity Tracking ◽  
Uptake Method

The vasculature of the mammalian renal medulla is complex, having neither discrete input nor output. There is also efficient countercurrent exchange between ascending and descending vasa recta in the vascular bundles. These considerations have hampered measurement of medullary blood flow since they impose pronounced constraints on methods used to assess flow. Three main strategies have been used: (i) indicator extraction; (ii) erythrocyte velocity tracking; and (iii) indicator dilution. These are discussed with respect to their assumptions, requirements, and limitations. There is a consensus that medullary blood flow is autoregulated, albeit over a narrower pressure range than is total renal blood flow. When normalized to gram tissue weight, medullary blood flow in the dog is similar to that in the rat, on the order of 1 to 1.5 mL∙min−1∙g−1. This is considerably greater than estimated by the radioiodinated albumin uptake method which has severe conceptual and practical problems. From both theoretical and experimental evidence it ssems that urinary concentrating ability is considerably less sensitive to changes in medullary blood flow than is often assumed.

Periodic changes of blood flow in the in vivo rat kidney

1979 ◽  
Vol 382 (1) ◽  
pp. 63-66 ◽  
Author(s):  
Paul Eggert ◽  
Volker Thiemann ◽  
Christoph Weiss
Keyword(s):  
Blood Flow ◽  
Rat Kidney ◽  
Periodic Changes

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.

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.

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