Autoregulation absent in normal kidney but present after renal damage

1960 ◽  
Vol 199 (3) ◽  
pp. 495-498 ◽  
Author(s):  
Jimmy B. Langston ◽  
Arthur C. Guyton ◽  
William J. Gillespie
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Blood Supply ◽  
Renal Damage ◽  
Perfusion Pressure ◽  
Lymphatic Drainage ◽  
Renal Ischemia ◽  
The Other ◽  
Surgical Trauma ◽  
Normal Kidney

Experiments of this study indicate that the kidney does not normally autoregulate its blood flow; in these experiments a change in perfusion pressure always resulted in a corresponding change in renal blood flow when the kidney was not subjected to surgical trauma. On the other hand, when renal ischemia was induced or when the perirenal tissues were intentionally damaged, autoregulation of renal blood flow occurred in every instance. Two possible theories are discussed for this autoregulation: a) blockage of the renal lymphatic drainage and b) disruption of the blood supply to the walls of the renal and intrarenal arteries.

scholarly journals Altered renal hemodynamics and impaired myogenic responses in the fawn-hooded rat

1999 ◽  
Vol 276 (3) ◽  
pp. R855-R863 ◽  
Author(s):  
Richard P. E. van Dokkum ◽  
Cheng-Wen Sun ◽  
Abraham P. Provoost ◽  
Howard J. Jacob ◽  
Richard J. Roman
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Damage ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Myogenic Response ◽  
Renal Perfusion Pressure ◽  
Medullary Blood Flow ◽  
Low Blood Pressure

The present study examined whether an abnormality in the myogenic response of renal arterioles that impairs autoregulation of renal blood flow (RBF) and glomerular capillary pressure (PGC) contributes to the development of renal damage in fawn-hooded hypertensive (FHH) rats. Autoregulation of whole kidney, cortical, and medullary blood flow and PGC were compared in young (12 wk old) FHH and fawn-hooded low blood pressure (FHL) rats in volume-replete and volume-expanded conditions. Baseline RBF, cortical and medullary blood flow, and PGCwere significantly greater in FHH than in FHL rats. Autoregulation of renal and cortical blood flow was significantly impaired in FHH rats compared with results obtained in FHL rats. Myogenically mediated autoregulation of PGC was significantly greater in FHL than in FHH rats. PGC rose from 46 ± 1 to 71 ± 2 mmHg in response to an increase in renal perfusion pressure from 100 to 150 mmHg in FHH rats, whereas it only increased from 39 ± 2 to 53 ± 1 mmHg in FHL rats. Isolated perfused renal interlobular arteries from FHL rats constricted by 10% in response to elevations in transmural pressure from 70 to 120 mmHg. In contrast, the diameter of vessels from FHH rats increased by 15%. These results indicate that the myogenic response of small renal arteries is altered in FHH rats, and this contributes to an impaired autoregulation of renal blood flow and elevations in PGC in this strain.

scholarly journals Blood Perfusion of the Kidney of Lophius Piscatorius L.

1953 ◽  
Vol 32 (2) ◽  
pp. 329-336 ◽  
Author(s):  
L. Brull ◽  
E. Nizet ◽  
E. B. Verney
Keyword(s):  
Blood Flow ◽  
Critical Level ◽  
Perfusion Pressure ◽  
Blood Perfusion ◽  
Urine Flow ◽  
The Other ◽  
Protein Nitrogen ◽  
Other Hand ◽  
Flow Through

Lophius kidneys perfused with the heparinized blood (venous) of the fish secrete urine in which total non-protein nitrogen is concentrated, magnesium highly concentrated, and chloride only slightly so or not at all. Oxygenation of the blood, or lowering the temperature of the perfusate from c. 20° to c. 5° C. does not appear to influence secretion. The blood flow through the kidneys increases with the perfusion pressure, the increase often becoming disproportionately large. The urine flow, on the other hand, above a certain critical level is largely independent of changes in perfusion pressure.

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.

Autoregulation of renal blood flow in the puppy

1975 ◽  
Vol 229 (4) ◽  
pp. 983-988 ◽  
Author(s):  
PA Jose ◽  
LM Slotkoff ◽  
S Montgomery ◽  
PL Calcagno ◽  
G Eisner
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Electromagnetic Flowmeter ◽  
Renin Angiotensin System ◽  
Renal Perfusion ◽  
Angiotensin System ◽  
Group Of Seven ◽  
Selective Blockade

The ability of the immature kidney to autoregulate blood flow was investigated. Renal blood flow was measured by electromagnetic flowmeter. In six puppies, selective blockade of the intrarenal effects of angiotensin II (AII) by [1-sarcosine, 8-alanine]angiotensin II (anti-AII) administered into the renal artery did not change renal blood flow. During selective renal AII blockade, intravenous AII raised perfusion pressure from 76 +/- 2 to 100 +/- 6 mmHg. Renal blood flow increased from 1.59 +/- 0.29 to 1.98 +/- 0.59 ml/g kidney per min, but returned to control levels within 40 s in spite of persistent arterial pressure elevation. In another group of seven puppies, renal blood flow remained constant despite reduction of renal perfusion pressure by aortic constriction to 60 mmHg. In two of these seven puppies intrarenal anti-AII did not abolish autoregulation. Autoregulation of renal blood flow occurs in the puppy and is not influenced by inhibition of angiotensin. The renin-angiotensin system does not appear to be involved in the normal regulation of renal blood flow in the puppy.

Mechanism of intrarenal blood flow redistribution after carotid artery occlusion

1977 ◽  
Vol 232 (2) ◽  
pp. F167-F172 ◽  
Author(s):  
E. H. Prosnitz ◽  
E. J. Zambraski ◽  
G. F. DiBona
Keyword(s):  
Blood Flow ◽  
Carotid Artery ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Artery Occlusion ◽  
Carotid Artery Occlusion ◽  
Outer Cortex ◽  
Renal Sympathetic Nerve Activity ◽  
Renal Perfusion Pressure

Bilateral carotid artery occlusion results in an increase in mean arterial pressure, an increase in renal sympathetic nerve activity, and a redistribution of renal blood flow from inner to outer cortex. To elucidate the mechanism of the renal blood flow redistribution, carotid artery occlusion was performed in anesthetized dogs with the left kidney either having renal perfusion pressure maintained constant (aortic constriction) or having alpha-adrenergic receptor blockade (phenoxybenzamine); the right kidney of the same dog served to document the normal response. When renal perfusion pressure was maintained constant, renal blood flow distribution (microspheres) was unchanged by carotid artery occlusion. In the presence of renal alpha-adrenergic receptor blockade, carotid artery occlusion elicited the usual redistribution of renal blood flow from inner to outer cortex. The redistribution of renal blood flow observed after carotid artery occlusion is mediated by the increase in renal perfusion pressure rather than the increase in renal sympathetic nerve activity.

Renal blood flow in dogs during diffusion respiration

1959 ◽  
Vol 14 (3) ◽  
pp. 405-410 ◽  
Author(s):  
Joseph E. Stone ◽  
Richard L. Irwin ◽  
Charles D. Wood ◽  
William B. Draper ◽  
Richard W. Whitehead
Keyword(s):  
Carbon Dioxide ◽  
Blood Flow ◽  
Medical Research ◽  
Renal Blood Flow ◽  
Renal Denervation ◽  
Respiratory Arrest ◽  
Renal Ischemia ◽  
Central Effects ◽  
Marked Decline ◽  
Series Of Experiments

Two series of experiments were performed with appropriate controls on dogs in which respiratory arrest was produced and maintained by the injection of an overdose of thiopental or by administration of decamethonium, respectively. Renal blood flow was measured by a modification of the method of Selkurt ( Methods in Medical Research, vol. 1). A marked fall in renal blood flow coincident with apnea and anuria was found to occur consistently with diffusion respiration under thiopental. Both the renal ischemia and the anuria were preventable by renal denervation (pharmacological block). During diffusion respiration experiments in which decamethonium was used to cause and maintain apnea, a marked decline in renal blood flow or urine secretion did not occur during the first 15 minutes of apnea. It is concluded that the prompt onset of anuria in diffusion respiration under thiopental is due to a central synergism between thiopental and endogenous carbon dioxide. Further, it is reasoned that the delayed fall in renal blood flow and attendant anuria which occurred under decamethonium represent the central effects of increasing concentrations of carbon dioxide in the absence of thiopental. Submitted on November 5, 1958

Effect of prostaglandin synthetase inhibitors on renal blood flow in the rat

1976 ◽  
Vol 231 (5) ◽  
pp. 1541-1545 ◽  
Author(s):  
WF Finn ◽  
WJ Arendshorst
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Small Diameter ◽  
Base Line ◽  
Sodium Pentobarbital ◽  
Prostaglandin Synthetase ◽  
Flow Transducer ◽  
Renal Vascular

Using a small-diameter electromagnetic flow transducer, the effect on the autoregulation of renal blood flow (RBF) of two structurally different prostaglandin synthetase inhibitors, indomethacin, 4 mg/kg BW, and meclofenamate, 5 mg/kg BW, was studied in nondiuretic rats anesthetized with either the oxybarbiturate, sodium pentobarbital, or the thiobarbiturate, Inactin. Regardless of the anesthetic agent, RBF remained relatively constant above a perfusion pressure of 105 mmHg. Treatment with either indomethacin or meclofenamate had no measurable effect on the autoregulatory response. Each agent, however, resulted in an increase in the renal vascular response to exogenous angiotensin II, an effect consistent with prostaglandin synthetase inhibition. Base-line RBF was significantly reduced by indomethacin or meclofenamate only in those animals that had previously received angiotensin. These results support the hypothesis that, in th rat, autoregulation of RBF occurs independently of prostaglandin activity, but that a relationship does exist between the renal vascular actions of angiotensin II and prostaglandins.

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