Role of the renal medulla in volume and arterial pressure regulation

1997 ◽  
Vol 273 (1) ◽  
pp. R1-R15 ◽  
Author(s):  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Fluid Pressure ◽  
Regulatory System ◽  
Renal Medulla ◽  
Water Excretion ◽  
Vasa Recta ◽  
Pressure Natriuresis ◽  
Total Renal Blood Flow

The original fascination with the medullary circulation of the kidney was driven by the unique structure of vasa recta capillary circulation, which Berliner and colleagues (Berliner, R. W., N. G. Levinsky, D. G. Davidson, and M. Eden. Am. J. Med. 24: 730-744, 1958) demonstrated could provide the economy of countercurrent exchange to concentrate large volumes of blood filtrate and produce small volumes of concentrated urine. We now believe we have found another equally important function of the renal medullary circulation. The data show that it is indeed the forces defined by Starling 100 years ago that are responsible for the pressure-natriuresis mechanisms through the transmission of changes of renal perfusion pressure to the vasa recta circulation. Despite receiving only 5-10% of the total renal blood flow, increases of blood flow to this region of the kidney cause a washout of the medullary urea gradient and a rise of the renal interstitial fluid pressure. These forces reduce tubular reabsorption of sodium and water, leading to a natriuresis and diuresis. Many of Starling's intrinsic chemicals, which he named "hormones," importantly modulate this pressure-natriuresis response by altering both the sensitivity and range of arterial pressure around which these responses occur. The vasculature of the renal medulla is uniquely sensitive to many of these vasoactive agents. Finally, we have found that the renal medullary circulation can play an important role in determining the level of arterial pressure required to achieve long-term fluid and electrolyte homeostasis by establishing the slope and set point of the pressure-natriuresis relationship. Measurable decreases of blood flow to the renal medulla with imperceptible changes of total renal blood flow can lead to the development of hypertension. Many questions remain, and it is now evident that this is a very complex regulatory system. It appears, however, that the medullary blood flow is a potent determinant of both sodium and water excretion and signals changes in blood volume and arterial pressure to the tubules via the physical forces that Professor Starling so clearly defined 100 years ago.

Sensitivity of the renal medullary circulation to plasma vasopressin

1996 ◽  
Vol 271 (3) ◽  
pp. R647-R653 ◽  
Author(s):  
K. G. Franchini ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Intravenous Infusion ◽  
Control Level ◽  
Flow Distribution ◽  
Renal Medulla ◽  
Urine Osmolality ◽  
Water Restriction ◽  
Doppler Flowmetry ◽  
Total Renal Blood Flow

Studies were carried out to determine the effects of physiological changes of plasma arginine vasopressin (AVP) on blood flow distribution in the renal cortex and medulla. Acute decerebration was performed so that studies could be carried out within the low physiological range of circulating AVP. Changes of renal cortical and medullary microcirculatory blood flow were measured with implanted optical fibers and laser-Doppler flowmetry, and total renal blood flow was measured with transit-time ultrasonography. During intravenous infusion of increasing doses of AVP, when plasma AVP was increased in steps from 2.9 to 11.2 pg/ml by intravenous infusion, mean arterial pressure (98 +/- 3 mmHg), total renal blood flow (8.2 +/- 0.6 ml. min-1.g kidney-1), and blood flow in the microcirculation of the cortex (2.11 +/- 0.28 V) remained unchanged, whereas that in the renal medulla decreased progressively. Medullary flow was significantly reduced when circulating levels of AVP increased from a control level of 2.8 to 5.0 pg/ml. The reductions of medullary flow were accompanied by parallel increases of urine osmolality. These data indicate that the vessels supplying the renal medullary circulation are sensitive within the range of plasma AVP concentrations observed with moderate water restriction. The medullary circulation exhibits a sensitivity AVP that parallels that found in the medullary collecting ducts.

Inner medullary blood flow in postischemic acute renal failure in the rat

1989 ◽  
Vol 256 (3) ◽  
pp. F456-F461 ◽  
Author(s):  
Y. Yagil ◽  
M. Miyamoto ◽  
R. L. Jamison
Keyword(s):  
Blood Flow ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Renal Ischemia ◽  
Renal Vascular Resistance ◽  
Left Renal Artery ◽  
Vasa Recta ◽  
Renal Vascular ◽  
Total Renal Blood Flow

To study the effect of renal ischemia on the circulation in the inner medulla, blood flow in descending and ascending vasa recta was determined by fluorescence videomicroscopy in the exposed papilla of the uninephrectomized rat after clamping of the renal artery for 45 min. Total renal blood flow was determined in parallel studies with an electromagnetic flowmeter. Animals were studied 90 min (group 1E) and 24 h (group 2E) after right nephrectomy and release of the left renal artery clamp. Control rats were studied 90 min (group 1C) and 24 h (group 2C) after right nephrectomy alone. In groups 1E and 2E, total renal blood flow was reduced to 70 and 80% of that in their respective controls; renal vascular resistance increased by 50 and 73%, respectively. In striking contrast, blood flow was markedly elevated in descending and ascending vasa recta in groups 1E and 2E compared with the values in their respective uninephrectomized controls. These results indicate that the circulation in the inner medulla is rapidly restored after 45 min of total renal ischemia and that vasa recta blood flow rises above normal after 90 min and 24 h, despite a reduction in total renal blood flow and an increase in renal vascular resistance.

Angiotensin II and prostaglandins in control of vasa recta blood flow

1988 ◽  
Vol 254 (3) ◽  
pp. F417-F424 ◽  
Author(s):  
W. A. Cupples ◽  
T. Sakai ◽  
D. J. Marsh
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Renal Medulla ◽  
Medullary Blood Flow ◽  
Vasa Recta ◽  
Electromagnetic Flow Probe ◽  
Angiotensin Blockade

Angiotensin II has been implicated in the regulation of medullary blood flow and is known to interact with prostaglandins at sites within the kidney. Therefore the role of angiotensin in control of vasa recta blood flow was studied in antidiuretic, Munich-Wistar rats. We also tested the hypothesis that prostaglandins act to modulate the effect of angiotensin. Total renal blood flow was measured by an electromagnetic flow probe, vasa recta blood flow by a dual-slit method. Captopril was used to confirm that angiotensin blockade increased renal blood flow (by 15 +/- 4%). Captopril and saralasin were used to show that angiotensin blockade increased vasa recta blood flow (by 23 +/- 9 and 14 +/- 7%, respectively). The results demonstrate a tonic constrictor effect of angiotensin in the renal medulla. Exogenous angiotensin II, delivered intravenously, failed to mimic the effect of endogenous angiotensin. Indomethacin did not alter blood pressure or renal blood flow but did reduce vasa recta blood flow by 20 +/- 3%, suggesting that prostaglandins act preferentially on the medullary circulation. Nor did it alter the response of blood pressure, of renal blood flow, or of vasa recta blood flow to captopril. Moreover, prior angiotensin blockade with either captopril or saralasin enhanced the medullary vasoconstrictor effect of indomethacin (P less than 0.05). These results are not consistent with the hypothesis that prostaglandins act primarily as angiotensin modulators. They suggest that the medullary interaction between angiotensin and prostaglandins differs from that in the cortex.

Vasopressin modulation of medullary blood flow and pressure-natriuresis-diuresis in the decerebrated rat

1997 ◽  
Vol 272 (5) ◽  
pp. R1472-R1479 ◽  
Author(s):  
K. G. Franchini ◽  
D. L. Mattson ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Fluid Pressure ◽  
Renal Medulla ◽  
Urinary Sodium Excretion ◽  
Water Restriction ◽  
Vascular Effects ◽  
Doppler Flowmetry ◽  
Physiological Importance ◽  
Medullary Blood Flow

Studies in our laboratory and others have demonstrated that arginine vasopressin (AVP) exerts potent vasoconstrictor actions on the vessels supplying the renal medulla. The physiological importance of these vascular effects of AVP has been difficult to assess because of high endogenous levels of AVP in anesthetized, surgically prepared animals. We have developed a decerebrated, hypophysectomized, renal-denervated rat model that enables us to study the effects of low levels of AVP on the pressure-diuresis, relationship under acute conditions. These rats maintain normal mean arterial pressure (MAP) and plasma AVP (2.5 pg/ml). Cortical and medullary blood flow (CBF and MBF, respectively) were measured by laser-Doppler flowmetry and total renal blood flow (RBF) by transit time flowmetry. Renal interstitial fluid pressure (RIFP) and urinary sodium excretion (UNaV) responses were determined during controlled increases of MAP produced by aortic occlusion below the renal arteries. From a baseline of 97 +/- 2 mmHg, 30% increases in MAP resulted in a 63% increase in MBF, 35% increase in RIFP, and sixfold increase in UNaV, whereas CBF and RBF remained unchanged. Infusion of AVP (0.50 ng.kg-1.min-1, which increased plasma AVP from normal control levels of 3 pg/ml to 11 pg/ml) produced no change in baseline MAP, RBF, or CBF but lowered MBF by 24%, RIFP by 26%, and UNaV by 71%. The slope of the relationship of AP and UNaV, MBF, and RIP was reduced to nearly zero by these small increases of plasma AVP. We conclude that an increase of plasma AVP in the range that occurs with water restriction decreases MBF selectively and greatly attenuates the arterial pressure-MBF and pressure-natriuretic relationship.

Measurement of Intrarenal Blood-Flow Distribution in the Rabbit Using Radioactive Microspheres

1975 ◽  
Vol 48 (1) ◽  
pp. 51-60 ◽  
Author(s):  
D. J. Warren ◽  
J. G. G. Ledingham
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Cortex ◽  
Flow Distribution ◽  
Rabbit Kidney ◽  
Radioactive Microspheres ◽  
Injection Dose ◽  
Intrarenal Blood Flow ◽  
Total Renal Blood Flow

1. Total renal blood flow and its distribution within the renal cortex of the conscious rabbit were studied with radioactive microspheres of 15 and 25 μm diameter. 2. The reliability of the microsphere technique was influenced by microsphere diameter and number (dose). The optimum microsphere diameter for determination of flow distribution in the rabbit kidney was 15 μm and dose 100–150 000 spheres. 3. Spheres of 15 μm nominal diameter were randomly distributed within the renal cortex of adult rabbits. The larger spheres in batches nominally 15 μm in diameter in young rabbits and 25 μm diameter in adult rabbits were preferentially distributed to the superficial cortex. 4. In adult rabbits 15 μm diameter spheres lodged in glomerular capillaries. Larger spheres occasionally lodged in interlobular arteries causing intrarenal haemorrhage. 5. Microspheres of 15 μm caused a decrease in renal clearance of creatinine and of p-aminohippurate when the total injection dose was about 200 000 spheres. These effects were greater when the injection dose was increased to 500 000 spheres. 6. The reduction in total renal blood flow observed with large doses of spheres largely reflected decreased outer cortical flow, as measured by a second injection of spheres, and confirmed by a decrease in p-aminohippurate extraction. 7. The reproducibility of multiple injection studies was limited by these intrarenal effects of microspheres. 8. Total renal blood flow measured in six rabbits in acute experiments by the microsphere technique was 107 ± 12 (mean±sd) ml/min and by p-aminohippurate clearance was 100 ± 10 ml/min. 9. Total renal blood flow in twelve conscious, chronically instrumented rabbits was 125 ± 11 ml/min, of which 92 ± 6 ml/min was distributed to the superficial cortex and 33 ± 4 ml/min to the deep cortex.

Contribution of renal nerves to renal blood flow variability during hemorrhage

1998 ◽  
Vol 274 (5) ◽  
pp. R1283-R1294 ◽  
Author(s):  
Simon C. Malpas ◽  
Roger G. Evans ◽  
Geoff A. Head ◽  
Elena V. Lukoshkova
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Spectral Power ◽  
Sympathetic Nerves ◽  
Renal Nerves ◽  
Similar Frequency ◽  
Blood Withdrawal ◽  
Conscious Rabbits ◽  
Renal Sympathetic

We have examined the role of the renal sympathetic nerves in the renal blood flow (RBF) response to hemorrhage in seven conscious rabbits. Hemorrhage was produced by blood withdrawal at 1.35 ml ⋅ min−1 ⋅ kg−1for 20 min while RBF and renal sympathetic nerve activity (RSNA) were simultaneously measured. Hemorrhage was associated with a gradual increase in RSNA and decrease in RBF from the 4th min. In seven denervated animals, the resting RBF before hemorrhage was significantly greater (48 ± 1 vs. 31 ± 1 ml/min intact), and the decrease in RBF did not occur until arterial pressure also began to fall (8th min); however, the overall percentage change in RBF by 20 min of blood withdrawal was similar. Spectral analysis was used to identify the nature of the oscillations in each variable. Before hemorrhage, a rhythm at ∼0.3 Hz was observed in RSNA, although not in RBF, whose spectrogram was composed mostly of lower-frequency (<0.25 Hz) components. The denervated group of rabbits had similar frequency spectrums for RBF before hemorrhage. RSNA played a role in dampening the effect of oscillations in arterial pressure on RBF as the transfer gain between mean arterial pressure (MAP) and RBF for frequencies >0.25 Hz was significantly less in intact than denervated rabbits (0.83 ± 0.12 vs. 1.19 ± 0.10 ml ⋅ min−1 ⋅ mmHg−1). Furthermore, the coherence between MAP and RBF was also significantly higher in denervated rabbits, suggesting tighter coupling between the two variables in the absence of RSNA. Before the onset of significant decreases in arterial pressure (up to 10 min), there was an increase in the strength of oscillations centered around 0.3 Hz in RSNA. These were accompanied by increases in the spectral power of RBF at the same frequency. As arterial pressure fell in both groups of animals, the dominant rhythm to emerge in RBF was centered between 0.15 and 0.20 Hz and was present in intact and denervated rabbits. It is speculated that this is myogenic in origin. We conclude that RSNA can induce oscillations in RBF at 0.3 Hz, plays a significant role in altering the effect of oscillations in arterial pressure on RBF, and mediates a proportion of renal vasoconstriction during hemorrhage in conscious rabbits.

Tubuloglomerular feedback dynamics and renal blood flow autoregulation in rats

1991 ◽  
Vol 260 (1) ◽  
pp. F53-F68 ◽  
Author(s):  
N. H. Holstein-Rathlou ◽  
A. J. Wagner ◽  
D. J. Marsh
Keyword(s):  
Blood Flow ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Slow Component ◽  
Broad Band ◽  
Experimental Results ◽  
Tubuloglomerular Feedback ◽  
Single Frequency ◽  
Vascular Control ◽  
Arterial Blood

To decide whether tubuloglomerular feedback (TGF) can account for renal autoregulation, we tested predictions of a TGF simulation. Broad-band and single-frequency perturbations were applied to arterial pressure; arterial blood pressure, renal blood flow and proximal tubule pressure were measured. Data were analyzed by linear systems analysis. Broad-band forcings of arterial pressure were also applied to the model to compare experimental results with simulations. With arterial pressure as the input and tubular pressure, renal blood flow, or renal vascular resistance as outputs, the model correctly predicted gain and phase only in the low-frequency range. Experimental results revealed a second component of vascular control active at 100-150 mHz that was not predicted by the simulation. Forcings at single frequencies showed that the system behaves linearly except in the band of 33-50 mHz in which, in addition, there are autonomous oscillations in TGF. Higher amplitude forcings in this band were attenuated by autoregulatory mechanisms, but low-amplitude forcings entrained the autonomous oscillations and provoked amplified oscillations in blood flow, showing an effect of TGF on whole kidney blood flow. We conclude that two components can be detected in the dynamic regulation of renal blood flow, i.e., a slow component that represents TGF and a faster component that most likely represents an intrinsic vascular myogenic mechanism.

Genetic co-segregation of renal haemodynamics and blood pressure in the spontaneously hypertensive rat

1988 ◽  
Vol 74 (1) ◽  
pp. 63-69 ◽  
Author(s):  
S. B. Harrap ◽  
A. E. Doyle
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Spontaneously Hypertensive Rat ◽  
Plasma Renin ◽  
Spontaneously Hypertensive

1. To determine the relevance of renal circulatory abnormalities found in the immature spontaneously hypertensive rat (SHR) to the genetic hypertensive process, glomerular filtration rate and renal blood flow were measured in conscious F2 rats, derived from crossbreeding SHR and normotensive Wistar–Kyoto rats (WKY), at 4, 11 and 16 weeks of age by determining the renal clearances of 51Cr-ethylenediaminetetra-acetate and 125I-hippuran respectively. Plasma renin activity was measured at 11 and 16 weeks of age. 2. Mean arterial pressure, glomerular filtration rate and renal blood flow increased between 4 and 11 weeks of age. Between 11 and 16 weeks the mean glomerular filtration rate and renal blood flow did not alter, although the mean arterial pressure rose significantly. At 11 weeks of age, during the developmental phase of hypertension, a significant negative correlation between mean arterial pressure and both glomerular filtration rate and renal blood flow was noted. However, by 16 weeks when the manifestations of genetic hypertension were more fully expressed, no correlation between mean arterial pressure and renal blood flow or glomerular filtration rate was observed. Plasma renin activity was negatively correlated with both glomerular filtration rate and renal blood flow, but the relationship was stronger at 11 than at 16 weeks of age. 3. These results suggest that the reduction in renal blood flow and glomerular filtration rate, found in immature SHR, is genetically linked to the hypertension and may be of primary pathogenetic importance. It is proposed that the increased renal vascular resistance in these young animals stimulates the rise of systemic arterial pressure which returns renal blood flow and glomerular filtration rate to normal.

Aortic blood flow subtraction: an alternative method for measuring total renal blood flow in conscious dogs

2002 ◽  
Vol 282 (5) ◽  
pp. R1528-R1535 ◽  
Author(s):  
N. C. F. Sandgaard ◽  
J. L. Andersen ◽  
N.-H. Holstein-Rathlou ◽  
P. Bie
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Aortic Blood Flow ◽  
Excretory Function ◽  
Endothelin 1 ◽  
Arterial Blood ◽  
Aortic Blood ◽  
Bilateral Carotid ◽  
Total Renal Blood Flow

We have measured total renal blood flow (TRBF) as the difference between signals from ultrasound flow probes implanted around the aorta above and below the renal arteries. The repeatability of the method was investigated by repeated, continuous infusions of angiotensin II and endothelin-1 seven times over 8 wk in the same dog. Angiotensin II decreased TRBF (350 ± 16 to 299 ± 15 ml/min), an effect completely blocked by candesartan (TRBF 377 ± 17 ml/min). Subsequent endothelin-1 infusion reduced TRBF to 268 ± 20 ml/min. Bilateral carotid occlusion (8 sessions in 3 dogs) increased arterial blood pressure by 49% and decreased TRBF by 12%, providing an increase in renal vascular resistance of 69%. Dynamic analysis showed autoregulation of renal blood flow in the frequency range <0.06–0.07 Hz, with a peak in the transfer function at 0.03 Hz. It is concluded that continuous measurement of TRBF by aortic blood flow subtraction is a practical and reliable method that allows direct comparison of excretory function and renal blood flow from two kidneys. The method also allows direct comparison between TRBF and flow in the caudal aorta.

Sign in / Sign up

Export Citation Format

Share Document