Effect of Hypoxia and Hypercapnic Acidosis on Renal Autoregulation in the Dog: Role of Renal Nerves

1983 ◽  
Vol 65 (5) ◽  
pp. 533-538 ◽  
Author(s):  
Robert J. Anderson ◽  
Richard G. Pluss ◽  
William T. Pluss ◽  
Jon Bell ◽  
Gary G. Zerbe
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Nerves ◽  
Hypercapnic Acidosis ◽  
Renal Perfusion Pressure

1. Previous studies suggest that hypoxia and hypercapnic acidosis exert a renal nerve mediated adverse effect on renal haemodynamic function. We therefore examined the effect of hypoxia and hypercapnic acidosis on renal blood flow and glomerular filtration rate responses to lowering renal perfusion pressure from 125 to 75 mmHg in the anaesthetized dog. To study the role of renal nerves in these responses, paired innervated and denervated kidneys were studied in each animal. 2. Hypoxia (Po2 43 ± 3 mmHg) affected neither renal blood flow nor glomerular filtration rate responses to decreasing renal perfusion pressure. 3. Hypercapnic acidosis (Pco2 71 ±2 mmHg; pH 7.03 ± 0.01) significantly decreased both renal blood flow and glomerular filtration rate as renal perfusion pressure was lowered. This effect of hypercapnic acidosis could be abolished by renal denervation. 4. These findings suggest that hypercapnic acidosis results in renal nerve stimulation, which prevents the usual decrease in renal afferent arteriolar tone that occurs in response to lowering of renal perfusion pressure.

Renal autoregulation of blood flow and filtration rate in the rabbit

1979 ◽  
Vol 237 (6) ◽  
pp. F479-F482 ◽  
Author(s):  
C. E. Ott ◽  
R. C. Vari
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Pressure Range ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Rabbit Kidney ◽  
Renal Perfusion Pressure

Electromagnetic flow techniques and inulin clearance were used to determine the autoregulatory capabilities of the rabbit kidney in vivo. Renal blood flow was measured in 13 animals over a renal perfusion pressure range of 40–110 mmHg. Normal renal blood flow averaged 3.2 +/- 0.3 ml.min-1.g kidney-1 and was efficiently autoregulated above a renal artery pressure of 75 mmHg. For every 10 mmHg renal pressure change above 75 mmHg renal blood flow changed only 0.96%. Renal perfusion pressure was reduced from 102 +/- 3 to 74 +/- 2 mmHg in six animals. Over this pressure range glomerular filtration rate was not significantly decreased and averaged 4.2 +/- 0.5 ml/min at high pressure compared to 4.0 +/- 0.5 ml/min at low perfusion pressure. Results show that the rabbit kidney autoregulates renal blood flow and glomerular filtration rate efficiently above 75 mmHg. This range of autoregulation compares well with the autoregulatory range of the dog. The results also show that in the autoregulatory range the rabbit and the rat appear to autoregulate with equal efficiency but that the rabbit kidney begins to autoregulate at a low perfusion pressure than the average of approximately 100 mmHg usually found in the rat.

Autoregulation of renal blood flow and glomerular filtration rate in the pregnant rabbit

1987 ◽  
Vol 252 (1) ◽  
pp. R69-R72 ◽  
Author(s):  
L. L. Woods ◽  
H. L. Mizelle ◽  
J. E. Hall
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Pregnant Rabbit ◽  
In Pregnancy

Our purpose was to determine whether renal autoregulatory capability is retained in pregnancy despite the marked renal vasodilation that occurs at this time. Renal blood flow and glomerular filtration rate (GFR) were measured in anesthetized pregnant (22–27 days gestation) and nonpregnant rabbits during step reductions in renal perfusion pressure from control (100 +/- 3 mmHg) to 50 mmHg. Control renal blood flow and GFR were significantly higher in pregnant animals, averaging 65 +/- 5 and 13.1 +/- 1.1 ml/min, respectively, compared with 50 +/- 5 and 9.4 +/- 1.2 ml/min in nonpregnant rabbits. Filtration fraction was also significantly elevated in pregnant animals (0.33 +/- 0.02 vs. 0.27 +/- 0.01 in nonpregnant rabbits). During step reductions in renal perfusion pressure, renal blood flow was well autoregulated down to approximately 70 mmHg in both nonpregnant and pregnant animals, falling by only 9 +/- 4 and 12 +/- 5%, respectively. Likewise, GFR was also well autoregulated, falling by 10 +/- 2 and 8 +/- 3% in nonpregnant and pregnant animals, respectively, when perfusion pressure was reduced from 90 to 70 mmHg. These results suggest that renal autoregulation is preserved in pregnancy despite the fact that the renal circulation is already markedly vasodilated.

Chronic Sodium-Potassium-ATPase Inhibition with Ouabain Impairs Renal Haemodynamics and Pressure Natriuresis in the Rat

1996 ◽  
Vol 91 (4) ◽  
pp. 497-502 ◽  
Author(s):  
Toshiaki Kurashina ◽  
Kent A. Kirchner ◽  
Joey P. Granger ◽  
Ami R. Patel
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Urinary Sodium Excretion ◽  
Renal Perfusion ◽  
Control Group ◽  
Renal Perfusion Pressure

1. Chronic Na+,K+-ATPase inhibition with ouabain induces hypertension in the rat. To examine the role of the kidney in this process, the effect of changes in renal perfusion pressure on glomerular filtration rate, renal blood flow and urinary sodium excretion were determined in rats treated intraperitoneally with ouabain (27.8 μg day−1 kg−1 body weight) or vehicle for 6 weeks. 2. After ouabain administration, baseline mean arterial pressure was significantly higher (P < 0.05) in ouabain-treated rats (151 ± 2 mmHg; n = 9) than in control rats (116 ± 4 mmHg; n = 8). 3. At equivalent renal perfusion pressures, glomerular filtration rate was significantly lower (P < 0.05) in ouabain-treated rats compared with control rats. Glomerular filtration rate was 721 ± 73μl/min at 150 mmHg, and fell significantly to 322 ± 64 μl/min at 100 mmHg. In the control group, glomerular filtration rate was well autoregulated. The glomerular filtration rate autoregulatory index was calculated to determine the ability to maintain glomerular filtration rate during changes in renal perfusion pressure (0 reflects perfect autoregulation; >1 reflects the absence of autoregulation). This index was greater in the ouabain group than in the control group (1.54 ± 0.2 compared with 0.29 ± 0.2; P < 0.05). Renal blood flow showed a similar pattern. 4. Absolute urinary sodium excretion rate was less in ouabain-treated rats than in control rats at equivalent renal perfusion pressures. The slope of the relationship between absolute urinary sodium excretion rate and renal perfusion pressure was greater (P < 0.05) in the control group than in the ouabain group (309.1 ± 57.1 compared with 82.1 ± 14.8 μmol min−1 mmHg−1). 5. Thus, chronic inhibition of Na+,K+-ATPase induces less efficient autoregulation of glomerular filtration rate and renal blood flow as well as a rightward shift in the pressure natriuresis relationship, such that a 25–30 mmHg higher renal perfusion pressure is necessary to excrete any given sodium load. These abnormalities may contribute to the development and maintenance of hypertension in this model.

Role of the Renal Nerves in Modulating Renin Release During Pressure Reduction at the Feline Kidney

1985 ◽  
Vol 69 (2) ◽  
pp. 185-195 ◽  
Author(s):  
Edward J. Johns
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renin Secretion ◽  
Renal Nerves ◽  
Pressure Reduction ◽  
Renal Perfusion Pressure

1. Experiments were undertaken in pentobarbitone-anaesthetized cats to determine how reflex activation of the renal nerves altered the responsiveness of the kidney to release renin during reductions in renal perfusion pressure. Reflex activation of the renal nerves was achieved by reducing carotid sinus perfusion pressure by 30 mmHg, which increased systemic blood pressure. During this period renal perfusion pressure was regulated at control levels and neither renal blood flow nor glomerular filtration rate changed, but there was a significant decrease in sodium excretion and increase in renin secretion. Renal denervation abolished both these latter responses. 2. Renal perfusion pressure reduction, by 25-30 mmHg, had no effect on renal blood flow or glomerular filtration rate but significantly decreased sodium excretion and increased renin secretion. Simultaneous reduction of carotid sinus and renal perfusion pressures had no effect on renal blood flow or glomerular filtration rate, decreased sodium excretion, and the magnitude of the increase in renin secretion was significantly greater than that obtained with reduction in renal perfusion pressure alone. Renal denervation abolished the increase in renin secretion during these manoeuvres. 3. During atenolol administration, renal haemodynamics and sodium excretion responses to renal pressure reduction were similar to those obtained in the absence of the drug. Renin secretion was increased, but significantly less than in the absence of atenolol. Simultaneous carotid sinus and renal pressure reductions during atenolol administration had no effect on renal haemodynamics, reduced sodium excretion and increased renin secretion, the magnitude of which was significantly greater than that recorded with only renal pressure reduction in the presence of atenolol. 4. Direct electrical stimulation of the renal nerves, at frequencies which caused a 5-10% reduction in renal blood flow, did not change glomerular filtration rate, decreased sodium excretion by 30% and increased the rate of renin secretion twofold. In the presence of atenolol, such renal nerve stimulation reduced renal blood flow to the same degree, did not change filtration rate, decreased sodium excretion by 37% but did not change renin secretion. 5. These results show that the magnitude of the release of renin in response to renal pressure reduction is dependent on activity within the renal nerves, being blunted after denervation, and enhanced during reflex activation of the renal nerves.

Use of a thermal pulse decay system to assess avian renal blood flow during reduced renal arterial perfusion pressure

1992 ◽  
Vol 262 (1) ◽  
pp. R90-R98 ◽  
Author(s):  
R. F. Wideman ◽  
R. P. Glahn ◽  
W. G. Bottje ◽  
K. R. Holmes
Keyword(s):  
Blood Flow ◽  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Regional Differences ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Portal Flow ◽  
Arterial Perfusion ◽  
Restricted Group

Using a simplified avian kidney model, renal arterial perfusion pressure (RAPP) was reduced from 120 (control) to 70 mmHg (near the glomerular filtration rate autoregulatory limit) and then to 46 mmHg (below the glomerular filtration rate autoregulatory range) in kidneys with ambient or partially restricted renal portal flow. Renal blood flow (RBF) was measured with a thermal pulse decay (TPD) system, using TPD thermistor probes inserted at three locations to evaluate regional differences in RBF. The clearance (CPAH) and extraction of p-aminohippuric acid were used to calculate renal plasma flow (RPF). CPAH, RPF, and RBF values were consistently lower for kidneys with restricted portal flow than for kidneys with ambient portal flow. Reducing RAPP to 46 mmHg did not significantly reduce CPAH, RPF, or RBF in the ambient group but did significantly reduce CPAH and RPF (regressed on RAPP) in the restricted group. RBF was not significantly affected when RAPP was reduced in the restricted group, although significant regional differences in blood flow were recorded. Renal vascular resistance decreased significantly as RAPP was reduced to 46 mmHg in the ambient group, confirming the renal autoregulatory response. In separate validation studies, significant reductions in RBF were detected by the TPD system during acute obstructions of portal and/or arterial flow. Overall, the results support previous evidence that avian RBF remains constant over a wide range of RAPPs. Observations of nonuniform intrarenal distributions of portal blood flow suggest that the portal system maintains the constancy of RBF in regions with proportionately high portal-to-arterial flow ratios.

Atrial appendectomy reduces ANF but not sodium excretion in acute vasopressin hypertension

1990 ◽  
Vol 258 (1) ◽  
pp. R77-R81
Author(s):  
R. S. Zimmerman ◽  
R. W. Barbee ◽  
A. Martinez ◽  
A. A. MacPhee ◽  
N. C. Trippodo
Keyword(s):  
Glomerular Filtration Rate ◽  
Glomerular Filtration ◽  
Sodium Excretion ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Sprague Dawley ◽  
Renal Perfusion Pressure ◽  
Sprague Dawley Rats ◽  
Circulating Levels

The present study was designed to determine whether atrial appendectomy would decrease the sodium excretion associated with pressor doses of arginine vasopressin (AVP) infusion in rats by decreasing circulating levels of atrial natriuretic factor (ANF). Ten to 21 days after either sham (n = 9) or bilateral atrial appendectomy (n = 13) AVP (19 ng.kg-1.min-1) was infused for 90 min in anesthetized Sprague-Dawley rats. Atrial appendectomy decreased circulating ANF levels from 469 +/- 70 pg/ml in sham-operated animals to 259 +/- 50 pg/ml (P less than 0.05) in atrial-appendectomized animals after 90 min of AVP infusion. Despite a reduction in circulating levels of ANF, sodium excretion, potassium excretion, and urine flow increased and were not affected by bilateral atrial appendectomy. Glomerular filtration rate and mean arterial pressure significantly increased in both groups of rats. The present study supports non-ANF factors such as increases in renal perfusion pressure and/or glomerular filtration rate as potential mechanisms in AVP-induced natriuresis.

Contralateral Natriuresis During Reduced Renal Artery Perfusion Pressure in "Renin-Depleted" Dogs

1972 ◽  
Vol 50 (3) ◽  
pp. 215-227
Author(s):  
L. J. Belleau ◽  
D. Mailhot
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Glomerular Filtration ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Plasma Renin ◽  
Systemic Blood Pressure ◽  
Renal Perfusion ◽  
Systemic Blood ◽  
Renal Perfusion Pressure

The mechanism of contralateral natriuresis subsequent to reduction of renal perfusion pressure was studied. In control dogs a drop in the renal perfusion pressure caused a very significant increase in the arterial and renal venous plasma renin activity, as well as a significant contralateral natriuresis. Systemic blood pressure increased along with contralateral intrarenal resistance. Glomerular filtration rate and renal blood flow did not change in the opposite kidney.In "renin-depleted" dogs a comparable drop in the renal perfusion pressure failed to stimulate renal venous and arterial plasma renin activity. Contralateral natriuresis increased significantly as well as the systemic blood pressure. In the absence of renin, intrarenal resistance of the opposite kidney did not change. Contralateral glomerular filtration rate and renal blood flow remained unchanged.During reduction of renal perfusion pressure, the most significant findings were: (1) absence of renin release despite the stimulation in renin-depleted dogs, (2) increase in contralateral resistance explained by the renin–angiotensin system, (3) systemic blood pressure increment despite renin release inhibition, and (4) the renin–angiotensin system not directly responsible for the contralateral natriuresis following a reduction in the renal perfusion pressure.Contralateral natriuresis cannot be explained by changes in glomerular filtration, renal blood flow, or intrarenal resistance. It is suggested that the rise in blood pressure or another factor, possibly neural or humoral, could explain the contralateral natriuresis.

scholarly journals Impaired autoregulation of renal blood flow in the fawn-hooded rat

1999 ◽  
Vol 276 (1) ◽  
pp. R189-R196 ◽  
Author(s):  
Richard P. E. Van Dokkum ◽  
Magdalena Alonso-Galicia ◽  
Abraham P. Provoost ◽  
Howard J. Jacob ◽  
Richard J. Roman
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Urinary Protein Excretion ◽  
Renal Perfusion Pressure ◽  
Protein Excretion ◽  
Low Blood Pressure ◽  
Renal Vascular

The responses to changes in renal perfusion pressure (RPP) were compared in 12-wk-old fawn-hooded hypertensive (FHH), fawn-hooded low blood pressure (FHL), and August Copenhagen Irish (ACI) rats to determine whether autoregulation of renal blood flow (RBF) is altered in the FHH rat. Mean arterial pressure was significantly higher in conscious, chronically instrumented FHH rats than in FHL rats (121 ± 4 vs. 109 ± 6 mmHg). Baseline arterial pressures measured in ketamine-Inactin-anesthetized rats averaged 147 ± 2 mmHg ( n = 9) in FHH, 132 ± 2 mmHg ( n = 10) in FHL, and 123 ± 4 mmHg ( n = 9) in ACI rats. Baseline RBF was significantly higher in FHH than in FHL and ACI rats and averaged 9.6 ± 0.7, 7.4 ± 0.5, and 7.8 ± 0.9 ml ⋅ min−1 ⋅ g kidney wt−1, respectively. RBF was autoregulated in ACI and FHL but not in FHH rats. Autoregulatory indexes in the range of RPPs from 100 to 150 mmHg averaged 0.96 ± 0.12 in FHH vs. 0.42 ± 0.04 in FHL and 0.30 ± 0.02 in ACI rats. Glomerular filtration rate was 20–30% higher in FHH than in FHL and ACI rats. Elevations in RPP from 100 to 150 mmHg increased urinary protein excretion in FHH rats from 27 ± 2 to 87 ± 3 μg/min, whereas it was not significantly altered in FHL or ACI rats. The percentage of glomeruli exhibiting histological evidence of injury was not significantly different in the three strains of rats. These results indicate that autoregulation of RBF is impaired in FHH rats before the development of glomerulosclerosis and suggest that an abnormality in the control of renal vascular resistance may contribute to the development of proteinuria and renal failure in this strain of rats.

Glomerular filtration dynamics during renal vasodilation with acetylcholine in the dog

1983 ◽  
Vol 244 (6) ◽  
pp. F606-F611 ◽  
Author(s):  
C. E. Thomas ◽  
C. E. Ott ◽  
P. D. Bell ◽  
F. G. Knox ◽  
L. G. Navar
Keyword(s):  
Glomerular Filtration Rate ◽  
Proximal Tubule ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Renal Perfusion Pressure ◽  
Effective Filtration Pressure ◽  
Single Nephron ◽  
Flow Dependency

The reason for the failure of glomerular filtration rate (GFR) to exhibit plasma flow dependency during pharmacologic vasodilation remains unclear although it has been suggested on the basis of experiments in rats that vasodilators may lead to a reduction in the glomerular filtration coefficient (Kf). To evaluate the applicability of this hypothesis to the dog, the effects of vasodilation with acetylcholine on glomerular dynamics and Kf were evaluated in two groups of dogs. One group (n = 19) was studied at spontaneous arterial pressures to allow maximum vasodilation to occur. In the other group (n = 5), renal arterial pressure was reduced and maintained at approximately 89 mmHg. Glomerular filtration rate and single nephron glomerular filtration rate were not altered significantly during acetylcholine infusion in either of the two groups. Both whole kidney and superficial filtration fractions decreased significantly. At spontaneous arterial pressures, transglomerular hydrostatic pressure was not altered significantly because of equivalent increases in proximal tubule pressure and in glomerular pressure. In the dogs studied at reduced renal perfusion pressure, glomerular capillary pressure did not change, but proximal tubule pressure increased slightly. Average effective filtration pressures and Kf were not significantly altered during the infusion of acetylcholine either at spontaneous or reduced renal perfusion pressures. These observations indicate that Kf in the dog is not significantly decreased by acetylcholine and that GFR is not affected during infusion of this agent because the effective filtration pressure is not significantly altered.

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