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.

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 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.

Relationship between renal perfusion pressure and blood flow in different regions of the kidney

1993 ◽  
Vol 264 (3) ◽  
pp. R578-R583 ◽  
Author(s):  
D. L. Mattson ◽  
S. Lu ◽  
R. J. Roman ◽  
A. W. Cowley
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Laser Doppler Flowmetry ◽  
Renal Cortex ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Doppler Flowmetry ◽  
Cortical Blood Flow ◽  
Renal Perfusion Pressure ◽  
Medullary Blood Flow

The present study examined the autoregulation of blood flow in different regions of the renal cortex and medulla in volume-expanded or hydropenic anesthetized rats. Blood flow was measured in the whole kidney by electromagnetic flowmetry, in the superficial cortex with implanted fibers and external probes for laser-Doppler flowmetry, and in the deep cortex and inner and outer medulla with implanted fibers for laser-Doppler flowmetry. At renal perfusion pressure > 100 mmHg, renal blood flow, superficial cortical blood flow, and deep cortical blood flow were all very well autoregulated in both volume-expanded and hydropenic rats. Inner and outer medullary blood flow were also well autoregulated in hydropenia, but blood flow in these regions was very poorly autoregulated in volume-expanded animals. As renal perfusion pressure was decreased below 100 mmHg in volume-expanded and hydropenic animals, renal blood flow, superficial and deep cortical blood flow, and inner and outer medullary blood flow all decreased. The results of these experiments demonstrate that blood flow in both the inner and outer portions of the renal medulla of the kidney is poorly autoregulated in volume-expanded rats but well autoregulated in hydropenic animals. In contrast, blood flow in all regions of the renal cortex is well autoregulated in both volume-expanded and hydropenic animals. These results suggest that changes in resistance in the postglomerular circulation of deep nephrons are responsible for the poor autoregulation of medullary blood flow in volume expansion despite well autoregulated cortical blood flow.

Influence of renal perfusion pressure on alpha- and beta-adrenergic stimulation of renin release

1985 ◽  
Vol 248 (3) ◽  
pp. E317-E326 ◽  
Author(s):  
M. L. Blair ◽  
Y. H. Chen ◽  
J. L. Izzo
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Neural Stimulation ◽  
Renin Release ◽  
Beta Blockade ◽  
Renal Perfusion Pressure ◽  
Stimulation Of ◽  
Total Renal Blood Flow

Experiments were performed in pentobarbital-anesthetized dogs to 1) determine if neural stimulation of renin release can be mediated by renal alpha-adrenoceptors at renal nerve stimulation (RNS) frequencies that have little or no effect on total renal blood flow (less than or equal to 1.2 Hz) and 2) ascertain whether alpha-adrenergic control of renin release is affected by renal perfusion pressure (RPP). The renal nerves were electrically stimulated both in the absence of RPP control and with RPP controlled near 85 mmHg. Decreased RPP lowered the threshold for neurogenic stimulation of renin release from less than or equal to 1.2 to 0.3 Hz. beta-Adrenoceptor blockade with propranolol blunted the renin secretion rate (RSR) response to graded RNS (0.3-5.0 Hz), but the extent of inhibition during low-frequency RNS was dependent on RPP. Propranolol prevented increased RSR at 0.6-1.2 Hz RNS when RPP was 111-120 mmHg but not when RPP was 85 mmHg. Combined alpha- and beta-blockade with prazosin and propranolol totally prevented increased RSR during 0.6-1.2 Hz RNS at reduced RPP. In summary, both alpha- and beta-adrenoceptors mediate neural stimulation of renin release at RNS frequencies that do not decrease total renal blood flow when RPP is 85 mmHg.

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.

Inhibition of renal vascular 20-HETE production impairs autoregulation of renal blood flow

1994 ◽  
Vol 266 (2) ◽  
pp. F275-F282 ◽  
Author(s):  
A. P. Zou ◽  
J. D. Imig ◽  
M. Kaldunski ◽  
P. R. Ortiz de Montellano ◽  
Z. Sui ◽  
...  
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Epoxyeicosatrienoic Acids ◽  
Blood Flows ◽  
Renal Perfusion Pressure ◽  
Renal Vascular

The present study evaluated the role of endogenous P-450 metabolites of arachidonic acid (AA) on autoregulation of renal blood flow in rats. Whole kidney and cortical blood flows were well autoregulated when renal perfusion pressure was varied from 150 to 100 mmHg. Infusion of 17-octadecynoic acid (17-ODYA) into the renal artery (33 nmol/min) increased cortical and papillary blood flows by 12.6 +/- 2.5 and 26.5 +/- 4.6%, respectively. After 17-ODYA, autoregulation of whole kidney and cortical blood flows was impaired. Intrarenal infusion of miconazole (8 nmol/min) had no effect on autoregulation of whole kidney, cortical, or papillary blood flows. 17-ODYA (1 microM) inhibited the formation of 20-hydroxyeicosatetraenoic acid (20-HETE) and 11,12- and 14,15-epoxyeicosatrienoic acids (EETs) by renal preglomerular microvessels in vitro by 83.7 +/- 7.4% and 89.0 +/- 4.9%, respectively. Miconazole (1 microM) reduced the formation of EETs by 86.4 +/- 5.7%, but it had no effect on the production of 20-HETE. These results suggest that endogenous P-450 metabolites of AA, particularly 20-HETE, may participate in the autoregulation of renal blood flow.

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.

scholarly journals Beneficial Effect of Serotonin 5-HT2-Receptor Antagonism on Renal Blood Flow Autoregulation in Cyclosporin-Treated Rats

1999 ◽  
Vol 10 (1) ◽  
pp. 28-34
Author(s):  
MARLEEN VERBEKE ◽  
JOHAN VAN DE VOORDE ◽  
LEO DE RIDDER ◽  
NORBERT LAMEIRE
Keyword(s):  
Blood Flow ◽  
Cyclosporin A ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Complete Loss ◽  
Intravenous Bolus ◽  
Renal Perfusion Pressure ◽  
Oxide Synthase ◽  
Renal Blood Flow Autoregulation

Abstract. Renal blood flow (RBF) autoregulation reappears in postischemic rat kidneys during serotonin (5-HT2) antagonism. The aim of the present study was to analyze whether 5-HT2 antagonism can ameliorate impaired RBF autoregulation in rats treated with 20 mg/kg per d cyclosporin A during 10 d. Autoregulation of RBF was assessed during stepwise lowering of renal perfusion pressure from 110 to 70 mmHg by gradual compression of the aorta. Autoregulation was lost in the cyclosporin A-treated rats. During administration of the 5-HT2 antagonist ritanserin (0.6 mg/kg intravenous bolus, followed by 1.2 mg/kg per h intravenous infusion during 1 h), autoregulation acutely reappeared. Intrarenal bolus injections of a selective 5-HT2-agonist, 2,5 dimethoxy-4-iodoamphetamine hydrochloride, elicited a significantly stronger renal vasocontraction in cyclosporin A-treated rats than in control rats. This finding was also observed with serotonin after nitric oxide-synthase blockade. These results (1) show the importance of 5-HT2-receptor-mediated vasoconstriction in the suppression of vasodilatory autoregulation of RBF in experimental cyclosporin A-induced renal dysfunction and (2) demonstrate that the complete loss of RBF autoregulation is not due to damage of the vascular smooth muscle cells.

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.

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