Renal Blood Flow Regulation

2012 ◽  
pp. 1964-1967
Author(s):  
William H. Shoff ◽  
Catherine T. Shoff ◽  
Suzanne M. Shepherd ◽  
Jonathan L. Burstein ◽  
Calvin A. Brown ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Flow Regulation ◽  
Blood Flow Regulation

A Control system model of renal blood flow regulation

1977 ◽  
Vol 10 (15) ◽  
pp. 76-82
Author(s):  
P.E. Cage ◽  
E.R. Carson ◽  
K.E. Britton
Keyword(s):  
Blood Flow ◽  
Control System ◽  
Renal Blood Flow ◽  
Flow Regulation ◽  
System Model ◽  
Blood Flow Regulation ◽  
Control System Model

Frequency encoding in renal blood flow regulation

2005 ◽  
Vol 288 (5) ◽  
pp. R1160-R1167 ◽  
Author(s):  
Donald J. Marsh ◽  
Olga V. Sosnovtseva ◽  
Alexey N. Pavlov ◽  
Kay-Pong Yip ◽  
Niels-Henrik Holstein-Rathlou
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Amplitude Modulation ◽  
Wavelet Transforms ◽  
Modulation Frequency ◽  
Flow Regulation ◽  
Tubuloglomerular Feedback ◽  
Conscious Rat ◽  
Blood Flow Regulation

With a model of renal blood flow regulation, we examined consequences of tubuloglomerular feedback (TGF) coupling to the myogenic mechanism via voltage-gated Ca channels. The model reproduces the characteristic oscillations of the two mechanisms and predicts frequency and amplitude modulation of the myogenic oscillation by TGF. Analysis by wavelet transforms of single-nephron blood flow confirms that both amplitude and frequency of the myogenic oscillation are modulated by TGF. We developed a double-wavelet transform technique to estimate modulation frequency. Median value of the ratio of modulation frequency to TGF frequency in measurements from 10 rats was 0.95 for amplitude modulation and 0.97 for frequency modulation, a result consistent with TGF as the modulating signal. The simulation predicted that the modulation was regular, while the experimental data showed much greater variability from one TGF cycle to the next. We used a blood pressure signal recorded by telemetry from a conscious rat as the input to the model. Blood pressure fluctuations induced variability in the modulation records similar to those found in the nephron blood flow results. Frequency and amplitude modulation can provide robust communication between TGF and the myogenic mechanism.

Renal blood flow regulation and arterial pressure fluctuations: a case study in nonlinear dynamics

1994 ◽  
Vol 74 (3) ◽  
pp. 637-681 ◽  
Author(s):  
N. H. Holstein-Rathlou ◽  
D. J. Marsh
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Deterministic Chaos ◽  
Flow Regulation ◽  
Whole Body ◽  
Thick Ascending Limb ◽  
Arterial Blood ◽  
Blood Flow Regulation ◽  
Wide Range

The arterial blood pressure, a physiological variable on which all renal excretory processes depend, fluctuates over a wide range of amplitudes and frequencies. Much of this variation originates in nonrenal vascular beds to support nonrenal tasks, and the fluctuations provide a noisy environment in which the kidney is obliged to operate. Were it not for renal blood flow autoregulation, it would be difficult to regulate renal excretory processes so as to maintain whole body variables within narrow bounds. Autoregulation is the noise filter on which other renal processes depend for maintaining a relatively noise-free environment in which to work. Because of the time-varying nature of the blood pressure, we have concentrated in this review on the now substantial body of work on the dynamics of renal blood flow regulation and the underlying mechanisms. Renal vascular control mechanisms are not simply reactive but have their own spontaneous dynamics. Both TGF and the myogenic mechanism oscillate autonomously. The TGF oscillation is the better understood of the two. There is an oscillation of tubular pressure, proximal tubular flow, early distal Cl- concentration, and efferent arteriolar blood flow at approximately 35 mHz; all these variables are synchronized when the measurements are made in a single tubule. The autonomous nature of the oscillation is supported by simulations of the nephron and its vasculature, which show that for a reasonable representation of the dynamics of these structures and of the parameters that govern their behavior, the solutions of the equation set are periodic at the frequency of the observed oscillation, and with the same phase relationships among its variables. The simulations also show that the critical variables for the development of the oscillation are the open-loop gain of the feedback system, and the various delays in the system of which convective transport in the axis of the thick ascending limb and signal transmission between the macula densa and the afferent arteriole are the most important. The oscillation in TGF is an example of nonlinear dynamical behavior and is yet another in a long list of oscillations and related dynamics arising in the inherently nonlinear properties of living systems. Some nonlinear systems can bifurcate to states known collectively as deterministic chaos, and TGF is a clear example of such a system. Rats with two different and unrelated forms of experimental hypertension provide tubular pressure records that pass statistical tests for ordered structure and sensitive dependence on initial conditions in the reconstructed state space, two of the hallmarks of deterministic chaos. These records also pass recent more stringent tests for chaos. The significance of deterministic chaos in the context of renal blood flow regulation is that the system regulating blood flow undergoes a physical change to a different dynamical state, and because the change is deterministic, there is every expectation that the critical change will yield itself to experimental discovery.(ABSTRACT TRUNCATED AT 400 WORDS)

A control system model of renal blood flow regulation

1981 ◽  
Vol 14 (4) ◽  
pp. 304-313 ◽  
Author(s):  
Peter E. Cage ◽  
Ewart R. Carson ◽  
Keith E. Britton
Keyword(s):  
Blood Flow ◽  
Control System ◽  
Renal Blood Flow ◽  
Flow Regulation ◽  
System Model ◽  
Blood Flow Regulation ◽  
Control System Model

DHHC21‐mediated α1 Adrenergic Receptor Palmitoylation Contributes to Renal Blood Flow Regulation During Sepsis

2020 ◽  
Vol 34 (S1) ◽  
pp. 1-1
Author(s):  
Xiaoyuan (Sherry) Yang ◽  
Ethan Zheng ◽  
Victor Chatterjee ◽  
Alexandria Creasy ◽  
Yonggang Ma ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Adrenergic Receptor ◽  
Flow Regulation ◽  
Blood Flow Regulation

Cellular transport ofl-arginine determines renal medullary blood flow in control rats, but not in diabetic rats despite enhanced cellular uptake capacity

2017 ◽  
Vol 312 (2) ◽  
pp. F278-F283 ◽  
Author(s):  
Patrik Persson ◽  
Angelica Fasching ◽  
Tom Teerlink ◽  
Peter Hansell ◽  
Fredrik Palm
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Cellular Uptake ◽  
Flow Regulation ◽  
Diabetic Rats ◽  
Uptake Capacity ◽  
Medullary Blood Flow ◽  
Arginine Uptake ◽  
Blood Flow Regulation

Diabetes mellitus is associated with decreased nitric oxide bioavailability thereby affecting renal blood flow regulation. Previous reports have demonstrated that cellular uptake of l-arginine is rate limiting for nitric oxide production and that plasma l-arginine concentration is decreased in diabetes. We therefore investigated whether regional renal blood flow regulation is affected by cellular l-arginine uptake in streptozotocin-induced diabetic rats. Rats were anesthetized with thiobutabarbital, and the left kidney was exposed. Total, cortical, and medullary renal blood flow was investigated before and after renal artery infusion of increasing doses of either l-homoarginine to inhibit cellular uptake of l-arginine or Nω-nitro- l-arginine methyl ester (l-NAME) to inhibit nitric oxide synthase. l-Homoarginine infusion did not affect total or cortical blood flow in any of the groups, but caused a dose-dependent reduction in medullary blood flow. l-NAME decreased total, cortical and medullary blood flow in both groups. However, the reductions in medullary blood flow in response to both l-homoarginine and l-NAME were more pronounced in the control groups compared with the diabetic groups. Isolated cortical tubular cells displayed similar l-arginine uptake capacity whereas medullary tubular cells isolated from diabetic rats had increased l-arginine uptake capacity. Diabetics had reduced l-arginine concentrations in plasma and medullary tissue but increased l-arginine concentration in cortical tissue. In conclusion, the reduced l-arginine availability in plasma and medullary tissue in diabetes results in reduced nitric oxide-mediated regulation of renal medullary hemodynamics. Cortical blood flow regulation displays less dependency on extracellular l-arginine and the upregulated cortical tissue l-arginine may protect cortical hemodynamics in diabetes.

Sign in / Sign up

Export Citation Format

Share Document