scholarly journals Impaired renal blood flow autoregulation in ischemic acute renal failure

1980 ◽  
Vol 18 (1) ◽  
pp. 68-76 ◽  
Author(s):  
Patricia L. Adams ◽  
Frederick F. Adams ◽  
P. Darwin Bell ◽  
L. Gabriel Navar
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Renal Blood Flow Autoregulation ◽  
Ischemic Acute Renal Failure

Effect of renal ischemia on cortical microsomal calcium accumulation

1985 ◽  
Vol 249 (5) ◽  
pp. C476-C483 ◽  
Author(s):  
A. Schieppati ◽  
P. D. Wilson ◽  
T. J. Burke ◽  
R. W. Schrier
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Artery ◽  
Renal Blood Flow ◽  
Normal Level ◽  
Mitochondrial Respiration ◽  
Renal Cortex ◽  
Bilateral Renal Artery ◽  
Ischemic Acute Renal Failure

Mitochondrial respiration, Ca2+ content, and Ca2+ kinetics have been found to be profoundly altered in ischemic acute renal failure (ARF). The effect of clamping the bilateral renal artery for 50 and 90 min on microsomal Ca2+ uptake was therefore examined in the rat. The 50-min clamping produced a reversible model of nonoliguric ARF, and the 90-min clamping produced a model of nonreversible oliguric ARF. In the 50-min nonoliguric model, ATP-dependent Ca2+ uptake by microsomes from renal cortex (nmol X mg protein-1 X 30 min-1) was significantly impaired immediately before release of the clamp and before return of renal blood flow (reflow) (191 +/- 11 vs. 83 +/- 11, P less than 0.005). However, in this nonoliguric model of ischemic ARF, microsomal uptake returned completely to normal after 1 h of reflow (sham 189 +/- 11 vs. 167 +/- 14 at 1 h, NS) and persisted at this normal level at 24 h (sham 166 +/- 14 vs. 150 +/- 13 at 24 h, NS). In the oliguric model of ARF the microsomal Ca2+ uptake also was impaired immediately after the clamp release (sham 191 +/- 11 vs. 93 +/- 11, P less than 0.001) as well as after 1 h of reflow (sham 189 +/- 11 vs. 129 +/- 12, P less than 0.005) but not at 24 h (sham 166 +/- 14 vs. 173 +/- 13, NS). The results indicate that impaired microsomal Ca2+ uptake occurs early in both oliguric and nonoliguric ARF and persists after 1 h of reflow in the oliguric model.(ABSTRACT TRUNCATED AT 250 WORDS)

Sympathetic nervous system in the loss of autoregulation in acute renal failure

1984 ◽  
Vol 246 (4) ◽  
pp. F379-F386 ◽  
Author(s):  
S. P. Kelleher ◽  
J. B. Robinette ◽  
J. D. Conger
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Nervous System ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Renal Denervation ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Renal Blood Flow Autoregulation

The responsiveness of the renal vascular system was investigated in uninephrectomized Sprague-Dawley rats in which acute renal failure had been induced by norepinephrine. The animals were studied at 1' and 3 wk after norepinephrine infusion. Uninephrectomized littermates served as controls. Compared with controls, there was an absence of renal blood flow autoregulation in 1-wk acute renal failure that returned in part by 3 wk. In 1-wk rats there was a marked increase, rather than decrease, in renovascular resistance as renal perfusion pressure was decreased. The renal vasculature was significantly less responsive in 1-wk rats than in control or 3-wk animals when acetylcholine, angiotensin II, or norepinephrine was infused into the renal artery at minimal vasoactive doses (all P less than 0.01). Paradoxically, renal vasoconstriction in response to renal nerve stimulation was greater in 1-wk than in 3-wk and control rats (P less than 0.01) and was not inhibited by renal artery infusion of phenoxybenzamine. Renal denervation significantly improved renal blood flow autoregulation in 1-wk animals (P less than 0.001) and completely abolished the increase in renovascular resistance as renal perfusion pressure was lowered. No effects of renal denervation on renal blood flow autoregulation were seen in control and 3-wk rats. It is concluded that renovascular responses to neurohumoral stimuli are aberrant in acute renal failure. The loss of renal blood flow autoregulation is related to an increased renovascular resistance that is due to increased activity of non-alpha-adrenergic mechanisms of the autonomic nervous system.

scholarly journals Dissociation of glomerular filtration and renal blood flow in HgCl2-induced acute renal failure

1982 ◽  
Vol 22 (2) ◽  
pp. 162-170 ◽  
Author(s):  
Raymond C. Vanholder ◽  
Marleen M. Praet ◽  
Piet A. Pattyn ◽  
Isidoor R. Leusen ◽  
Norbert H. Lameire
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Glomerular Filtration ◽  
Renal Blood Flow

Reduced renal blood flow in early cisplatin-induced acute renal failure in the rat

1985 ◽  
Vol 249 (4) ◽  
pp. F490-F496 ◽  
Author(s):  
J. A. Winston ◽  
R. Safirstein
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Plasma Flow ◽  
Volume Expansion ◽  
Filtration Rate ◽  
Renal Plasma Flow ◽  
Single Nephron ◽  
Renal Vascular

Studies were designed to determine the cause of the reduced glomerular filtration rate (GFR) in early cisplatin-induced acute renal failure. Rats were studied 72 h following a single intraperitoneal injection of cisplatin (5 mg/kg) or vehicle (0.9% NaCl). Whole kidney GFR and blood flow were lower in cisplatin-treated animals than in controls (0.30 +/- 0.06 vs. 1.17 +/- 0.06 ml X min-1 X g kidney wt-1 and 5.30 +/- 0.62 vs. 8.25 +/- 0.43 ml X min-1 X g kidney wt-1, respectively; P less than 0.001), as were superficial nephron GFR and stop-flow pressure (20.2 +/- 2.1 vs. 34.5 +/- 2.0 nl X min-1 X g kidney wt-1 and 29.0 +/- 1.9 vs. 39.8 +/- 1.3 mmHg, respectively; P less than 0.001). After volume expansion, renal plasma flow increased in control rats, whereas whole kidney and single nephron GFR did not change. In experimental animals, whole kidney filtration rate rose to 0.58 +/- 0.07 ml X min-1 X g kidney wt-1, single nephron filtration rate increased to 29.9 +/- 3.5 nl X min-1 X g kidney wt-1 (P less than 0.005), and renal plasma flow increased to 5.62 +/- 0.60 ml X min-1 X g kidney wt-1 (P less than 0.05). Intratubular hydrostatic pressure was not different in the two groups before or after volume expansion. The results of these studies show that the reduced GFR in early cisplatin-induced renal failure is due, in part, to reversible changes in renal blood flow and renal vascular resistance.

Cardiac Output, Renal Blood Flow and Hepatic Blood Flow in Rats with Glycerol-Induced Acute Renal Failure

Nephron ◽  
1989 ◽  
Vol 53 (4) ◽  
pp. 353-357 ◽  
Author(s):  
T. Kishimoto ◽  
W. Sakamoto ◽  
T. Nakatani ◽  
T. Ito ◽  
K. Iwai ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Cardiac Output ◽  
Renal Blood Flow ◽  
Hepatic Blood Flow

Noninvasive monitoring of renal blood flow characteristics during acute renal failure in man

1990 ◽  
Vol 16 (3) ◽  
pp. 153-158 ◽  
Author(s):  
P. E. Stevens ◽  
S. J. Gwyther ◽  
M. E. Hanson ◽  
J. E. Boultbee ◽  
W. J. Kox ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Renal Blood Flow ◽  
Flow Characteristics ◽  
Noninvasive Monitoring

High-NaCl diet impairs dynamic renal blood flow autoregulation in rats with adenine-induced chronic renal failure

2014 ◽  
Vol 306 (6) ◽  
pp. R411-R419 ◽  
Author(s):  
Aso Saeed ◽  
Gerald F. DiBona ◽  
Elisabeth Grimberg ◽  
Lisa Nguy ◽  
Minne Line Nedergaard Mikkelsen ◽  
...  
Keyword(s):  
Renal Failure ◽  
Blood Flow ◽  
Chronic Renal Failure ◽  
Arterial Pressure ◽  
Renal Blood Flow ◽  
Low Frequency ◽  
Organ Injury ◽  
Myogenic Response ◽  
Frequency Range ◽  
Renal Blood Flow Autoregulation

This study examined the effects of 2 wk of high-NaCl diet on kidney function and dynamic renal blood flow autoregulation (RBFA) in rats with adenine-induced chronic renal failure (ACRF). Male Sprague-Dawley rats received either chow containing adenine or were pair-fed an identical diet without adenine (controls). After 10 wk, rats were randomized to either remain on the same diet (0.6% NaCl) or to be switched to high 4% NaCl chow. Two weeks after randomization, renal clearance experiments were performed under isoflurane anesthesia and dynamic RBFA, baroreflex sensitivity (BRS), systolic arterial pressure variability (SAPV), and heart rate variability were assessed by spectral analytical techniques. Rats with ACRF showed marked reductions in glomerular filtration rate and renal blood flow (RBF), whereas mean arterial pressure and SAPV were significantly elevated. In addition, spontaneous BRS was reduced by ∼50% in ACRF animals. High-NaCl diet significantly increased transfer function fractional gain values between arterial pressure and RBF in the frequency range of the myogenic response (0.06–0.09 Hz) only in ACRF animals (0.3 ± 4.0 vs. −4.4 ± 3.8 dB; P < 0.05). Similarly, a high-NaCl diet significantly increased SAPV in the low-frequency range only in ACRF animals. To conclude, a 2-wk period of a high-NaCl diet in ACRF rats significantly impaired dynamic RBFA in the frequency range of the myogenic response and increased SAPV in the low-frequency range. These abnormalities may increase the susceptibility to hypertensive end-organ injury and progressive renal failure by facilitating pressure transmission to the microvasculature.

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