scholarly journals Analysis of the critical determinants of renal medullary oxygenation

2019 ◽  
Vol 317 (6) ◽  
pp. F1483-F1502 ◽  
Author(s):  
Chang-Joon Lee ◽  
Bruce S. Gardiner ◽  
Roger G. Evans ◽  
David W. Smith
Keyword(s):  
Cardiopulmonary Bypass ◽  
Volume Expansion ◽  
Perfusion Pressure ◽  
Isotonic Saline ◽  
Extracellular Fluid ◽  
Renal Medulla ◽  
Renal Perfusion ◽  
Outer Medulla ◽  
Renal Perfusion Pressure ◽  
Medullary Tissue

We have previously developed a three-dimensional computational model of oxygen transport in the renal medulla. In the present study, we used this model to quantify the sensitivity of renal medullary oxygenation to four of its major known determinants: medullary blood flow (MBF), medullary oxygen consumption rate (V̇o2,M), hemoglobin (Hb) concentration in the blood, and renal perfusion pressure. We also examined medullary oxygenation under special conditions of hydropenia, extracellular fluid volume expansion by infusion of isotonic saline, and hemodilution during cardiopulmonary bypass. Under baseline (normal) conditions, the average medullary tissue Po2 predicted for the whole renal medulla was ~30 mmHg. The periphery of the interbundle region in the outer medulla was identified as the most hypoxic region in the renal medulla, which demonstrates that the model prediction is qualitatively accurate. Medullary oxygenation was most sensitive to changes in renal perfusion pressure followed by Hb, MBF, and V̇o2,M, in that order. The medullary oxygenation also became sensitized by prohypoxic changes in other parameters, leading to a greater fall in medullary tissue Po2 when multiple parameters changed simultaneously. Hydropenia did not induce a significant change in medullary oxygenation compared with the baseline state, while volume expansion resulted in a large increase in inner medulla tissue Po2 (by ~15 mmHg). Under conditions of cardiopulmonary bypass, the renal medulla became severely hypoxic, due to hemodilution, with one-third of the outer stripe of outer medulla tissue having a Po2 of <5 mmHg.

scholarly journals Osmotic hypertonicity of the renal medulla during changes in renal perfusion pressure in the rat

1998 ◽  
Vol 508 (3) ◽  
pp. 929-935 ◽  
Author(s):  
Leszek Dobrowolski ◽  
Bozena Badzynska ◽  
Agnieszka Walkowska ◽  
Janusz Sadowski
Keyword(s):  
Perfusion Pressure ◽  
Renal Medulla ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure

Saline-Induced Natriuresis in the Dog without Prior Exposure of the Kidney to the Physical Effects of Expansion of the Extracellular Fluid Compartment

1978 ◽  
Vol 54 (5) ◽  
pp. 525-527
Author(s):  
P. J. Klemmer ◽  
C. De Los Santos ◽  
W. B. Blythe
Keyword(s):  
Perfusion Pressure ◽  
Control Period ◽  
Extracellular Fluid ◽  
Renal Perfusion ◽  
Prior Exposure ◽  
Renal Perfusion Pressure ◽  
Fluid Compartment ◽  
Isotonic Sodium Chloride ◽  
Physical Effects ◽  
Filtered Load

1. Experiments were carried out in dogs in which renal perfusion pressure was reduced 40 min before beginning expansion of the extracellular fluid space by 10% with isotonic sodium chloride solution. Sodium excretion increased up to 590% of control values in spite of the fact that the filtered load of sodium was below that of the control period and circulating mineralocorticoids were not suppressed. 2. The findings indicate that, in the dog, prior exposure of the kidney to the volume-expanded state is not a prerequisite for natriuresis to occur.

scholarly journals Cortical and medullary hemodynamics in deoxycorticosterone acetate-salt hypertensive mice.

1998 ◽  
Vol 9 (3) ◽  
pp. 346-354 ◽  
Author(s):  
V Gross ◽  
A Lippoldt ◽  
J Bohlender ◽  
M Bader ◽  
A Hansson ◽  
...  
Keyword(s):  
Blood Flow ◽  
Volume Expansion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Kidney Weight ◽  
Cortical Blood Flow ◽  
Renal Perfusion Pressure ◽  
Medullary Blood Flow ◽  
Saline Loading ◽  
Baseline Values

The effect of acutely increasing renal perfusion pressure or extracellular fluid volume on renal medullary and cortical blood flow was examined in the low-renin deoxycorticosterone acetate (DOCA)-salt hypertension model in mice. A 50-mg DOCA tablet was implanted, and 1% saline was given as drinking water for 3 wk. Medullary and cortical blood flow were determined with laser-Doppler flowmetry, and whole-kidney blood flow was measured with a transit-time ultrasound flowprobe around the renal artery. In control mice, total renal blood flow ranged from 6.3 and 7.6 ml/min per g kidney weight and in DOCA-salt mice from 4.3 and 4.7 ml/min per g kidney weight, respectively, and was minimally affected as renal perfusion pressure was increased. Renal vascular resistance increased correspondingly. During stepwise increases in renal artery pressure from 90 to 140 mmHg, medullary blood flow progressively increased in control mice to 125% of baseline values, whereas cortical blood flow did not change. In DOCA-salt mice, increasing BP from 100 to 154 mmHg had no effect on either cortical or medullary blood flow. Urine flow and sodium excretion were lower in DOCA-salt mice than in controls and increased nearly to the same extent in both groups after volume expansion with isotonic saline. Total renal blood flow increased after saline loading, more in controls than in DOCA-salt mice. Increases in medullary blood flow after saline loading were up to 122% of baseline values in controls and demonstrated a significantly steeper slope than the 110% of baseline increases in DOCA-salt mice. Cortical blood flow, however, was not different between the groups. Thus, medullary blood flow is not as tightly autoregulated as cortical blood flow in normal mice. Natriuresis with acute volume loading is facilitated by increased medullary blood flow. In DOCA-salt mice, the medullary blood flow reaction to renal perfusion pressure increases is abolished, whereas flow increases with extracellular volume expansion are diminished. These results suggest that diminished pressure-natriuresis responses in DOCA-salt mice are related to perturbed medullary blood flow.

Impaired Transmission of Pressure to the Renal Interstitium in Spontaneous Hypertension

Physiology ◽  
1992 ◽  
Vol 7 (1) ◽  
pp. 23-26
Author(s):  
AA Khraibi
Keyword(s):  
Hydrostatic Pressure ◽  
Volume Expansion ◽  
Spontaneously Hypertensive Rats ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Renal Perfusion Pressure ◽  
Renal Interstitium ◽  
Wistar Kyoto

In Okamoto spontaneously hypertensive rats, compared with control Wistar-Kyoto rats, natriuretic and diuretic responses to increases in renal perfusion pressure are attenuated but with acute saline volume expansion they are exaggerated. The extent of elevations in renal interstitial hydrostatic pressure appears to determine the natriuretic and diuretic responses.

Effect of Renal Perfusion Pressure on Renal Interstitial Hydrostatic Pressure and Sodium Excretion

Hypertension ◽  
1995 ◽  
Vol 25 (4) ◽  
pp. 866-871 ◽  
Author(s):  
Tetsuya Nakamura ◽  
Tetsuo Sakamaki ◽  
Toshiaki Kurashina ◽  
Kunio Sato ◽  
Zenpei Ono ◽  
...  
Keyword(s):  
Hydrostatic Pressure ◽  
Sodium Excretion ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure

Selective neuronal nitric oxide synthase inhibition blocks furosemide-stimulated renin secretion in vivo

1995 ◽  
Vol 269 (1) ◽  
pp. F134-F139 ◽  
Author(s):  
W. H. Beierwaltes
Keyword(s):  
Nitric Oxide ◽  
Blood Pressure ◽  
Nitric Oxide Synthase ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Macula Densa ◽  
Renin Secretion ◽  
Renal Perfusion Pressure ◽  
Neuronal Nos ◽  
Oxide Synthase

The macula densa is a regulatory site for renin. It contains exclusively the neuronal isoform of nitric oxide synthase (NOS), suggesting NO could stimulate renin secretion through the macula densa pathway. To test whether neuronal NOS mediates renin secretion, renin was stimulated by either the renal baroreceptor or the diuretic furosemide (acting through the macula densa pathway). Renin secretion rate (RSR) was measured in 12 Inactin-anesthetized rats at normal (104 +/- 3 mmHg) and reduced renal perfusion pressure (65 +/- 1 mmHg), before and after selective blockade of the neuronal NOS with 7-nitroindazole (7-NI, 50 mg/kg ip). 7-NI had no effect on basal blood pressure (102 +/- 2 mmHg) or renal blood flow (RBF). Decreasing renal perfusion pressure doubled RSR from 11.8 +/- 3.3 to 22.9 +/- 5.7 ng ANG I.h-1.min-1 (P < 0.01) (ANG I is angiotensin I). Similarly, in 7-NI-treated rats, reduced perfusion doubled RSR from 8.5 +/- 1.8 to 20.5 +/- 6.2 ng ANG I.h-1.min-1 (P < 0.01). Renal hemodynamics and RSR were measured in response to 5 mg/kg iv furosemide in 12 control rats and 11 rats treated with 7-NI. Blocking neuronal NOS did not alter blood pressure (102 +/- 2 mmHg), RBF (5.8 +/- 0.4 ml.min-1.g kidney wt-1), or renal vascular resistance (18.7 +/- 1.4 mmHg.ml-1.min.g kidney wt).(ABSTRACT TRUNCATED AT 250 WORDS)

Membrane potential measurements in renal afferent and efferent arterioles: actions of angiotensin II

1997 ◽  
Vol 273 (2) ◽  
pp. F307-F314 ◽  
Author(s):  
R. Loutzenhiser ◽  
L. Chilton ◽  
G. Trottier
Keyword(s):  
Angiotensin Ii ◽  
Perfusion Pressure ◽  
Rat Kidney ◽  
Renal Perfusion ◽  
Membrane Potentials ◽  
Ang Ii ◽  
Ca Channels ◽  
Renal Perfusion Pressure

An adaptation of the in vitro perfused hydronephrotic rat kidney model allowing in situ measurement of arteriolar membrane potentials is described. At a renal perfusion pressure of 80 mmHg, resting membrane potentials of interlobular arteries (22 +/- 2 microns) and afferent (14 +/- 1 microns) and efferent arterioles (12 +/- 1 microns) were -40 +/- 2 (n = 8), -40 +/- 1 (n = 45), and -38 +/- 2 mV (n = 22), respectively (P = 0.75). Using a dual-pipette system to stabilize the impalement site, we measured afferent and efferent arteriolar membrane potentials during angiotensin II (ANG II)-induced vasoconstriction. ANG II (0.1 nM) reduced afferent arteriolar diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.005) and membrane potentials from -40 +/- 2 to -29 +/- mV (P = 0.012). ANG II elicited a similar vasoconstriction in efferent arterioles, decreasing diameters from 13 +/- 1 to 8 +/- 1 microns (n = 8, P = 0.004), but failed to elicit a significant depolarization (-39 +/- 2 for control; -36 +/- 3 mV for ANG II; P = 0.27). Our findings thus indicate that resting membrane potentials of pre- and postglomerular arterioles are similar and lie near the threshold activation potential for L-type Ca channels. ANG II-induced vasoconstriction appears to be closely coupled to membrane depolarization in the afferent arteriole, whereas mechanical and electrical responses appear to be dissociated in the efferent arteriole.

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