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.

Human renal response to meat meal

1986 ◽  
Vol 250 (4) ◽  
pp. F613-F618 ◽  
Author(s):  
T. H. Hostetter
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Renal Plasma Flow ◽  
Statistical Significance ◽  
Prostaglandin E ◽  
Base Line ◽  
Meat Meal ◽  
Time Period ◽  
Beef Steak ◽  
Renal Vascular

Glomerular filtration rate (GFR) increases after a meat meal in several species. The mechanism of this phenomenon is unknown and the excretory and metabolic responses largely unexplored. We examined in humans the nature of the hemodynamic response to a meat meal, the role of salt and water load in this response, and the associated renal excretory responses. Ten normal volunteers were studied after eating an average of 3.5 g/kg body wt of lean cooked beef steak and, on a separate day, after ingesting an amount of sodium and water equivalent to that in the steak. Average GFR increased by 28% for the entire 3 h after the meat meal compared with the same time period after the control salt solution (90 +/- 8 vs. 114 +/- 6 ml X min-1 X 1.73 M-2, mean +/- SE, P less than 0.05) and by 15% compared with the base-line periods, although this difference was not of statistical significance. However, not all subjects demonstrated an increase, and in those eight who did the degree was variable from 5 to 46% for the 3-h mean above the basal value. During the hour of peak GFR, the increment was associated with a nearly proportional increase in renal plasma flow and renal blood flow (all P less than 0.05). The increase in renal blood flow was entirely due to a significant fall in renal vascular resistance. The vasodilation was not accompanied by any change in prostaglandin E excretion.(ABSTRACT TRUNCATED AT 250 WORDS)

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.

Renal vasodilatation after inhibition of renin or converting enzyme in marmoset

1986 ◽  
Vol 251 (5) ◽  
pp. H897-H902
Author(s):  
D. Neisius ◽  
J. M. Wood ◽  
K. G. Hofbauer
Keyword(s):  
Blood Pressure ◽  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Vascular Resistance ◽  
Enzyme Inhibitor ◽  
Renal Vascular Resistance ◽  
Converting Enzyme ◽  
Renin Inhibition ◽  
Renal Vascular

The relative importance of angiotensin II for the renal vasodilatory response after converting-enzyme inhibition was evaluated by a comparison of the effects of converting-enzyme and renin inhibition on renal vascular resistance. Renal, mesenteric, and hindquarter blood flows were measured with chronically implanted ultrasonic-pulsed Doppler flow probes in conscious, mildly volume-depleted marmosets after administration of a converting-enzyme inhibitor (enalaprilat, 2 mg/kg iv), a synthetic renin inhibitor (CGP 29,287, 1 mg/kg iv), or a renin-inhibitory monoclonal antibody (R-3-36-16, 0.1 mg/kg iv). Enalaprilat reduced blood pressure (-16 +/- 4 mmHg, n = 6) and induced a selective increase in renal blood flow (27 +/- 8%, n = 6). CGP 29,287 and R-3-36-16 induced comparable reductions in blood pressure (-16 +/- 4 mmHg, n = 6 and -20 +/- 4 mmHg, n = 5, respectively) and selective increases in renal blood flow (36 +/- 12%, n = 6 and 34 +/- 16%, n = 4, respectively). The decrease in renal vascular resistance was of similar magnitude for all of the inhibitors (enalaprilat -28 +/- 3%, CGP 29,287 -32 +/- 6%; and R-3-36-16 -33 +/- 7%). These results indicate that the renal vasodilatation induced after converting-enzyme or renin inhibition is mainly due to decreased formation of angiotensin II.

Cyclosporine augments renal but not systemic vascular reactivity

1990 ◽  
Vol 258 (1) ◽  
pp. F211-F217
Author(s):  
M. D. Garr ◽  
M. S. Paller
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Renal Blood Flow ◽  
Arginine Vasopressin ◽  
Vascular Reactivity ◽  
Pressor Response ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Vascular Responsiveness ◽  
Renal Vascular

Renal vasoconstriction and hypertension are major side effects of cyclosporine. We tested the acute effects of cyclosporine on renal and systemic vascular reactivity to norepinephrine, angiotensin II, and arginine vasopressin. Renal vascular reactivity was tested in anesthetized Sprague-Dawley rats with denervated kidneys. Renal blood flow was measured with an electromagnetic flow probe in response to graded intra-arterial infusions of vasoconstrictors before and after intravenous administration of cyclosporine. Cyclosporine augmented the decrease in renal blood flow and the increase in renal vascular resistance produced by intrarenal norepinephrine, angiotensin II, and arginine vasopressin. In these studies, systemic blood pressure did not change and cyclosporine caused no direct change in basal renal blood flow. In contrast, in conscious animals, cyclosporine did not increase the pressor response to intravenous norepinephrine or to angiotensin II. Rather, cyclosporine caused enhanced baroreflex slowing of heart rate and a decrease in the pressor response to both norepinephrine and angiotensin II. Even when the baroreceptor reflex was blocked by pentolinium, the pressor response to norepinephrine in cyclosporine-treated animals was diminished compared with vehicle-treated animals. Therefore, although cyclosporine augmented renal vasoconstriction in response to norepinephrine, angiotensin II, and arginine vasopressin, it did not acutely increase the systemic vascular response to these agents. Enhanced renal vascular responsiveness is an additional mechanism for cyclosporine-mediated renal vasoconstriction. Lack of enhanced peripheral vascular responsiveness suggests that hypertension is not likely to be due to direct effects on the systemic vasculature and is more likely to be a consequence of renal functional impairment.

Renal blood flow autoregulation in developing swine

1983 ◽  
Vol 245 (1) ◽  
pp. H1-H6 ◽  
Author(s):  
N. M. Buckley ◽  
P. Brazeau ◽  
I. D. Frasier
Keyword(s):  
Blood Flow ◽  
Steady State ◽  
Renal Blood Flow ◽  
Perfusion Pressure ◽  
Left Renal Artery ◽  
Inferior Vena Caval ◽  
In Situ Perfusion ◽  
Renal Vascular ◽  
Renal Blood Flow Autoregulation

Pressure-flow relationships (P/F) in the renal circulation were determined in 62 swine, aged 1 day-2 mo, anesthetized with pentobarbital sodium. Aortic and inferior vena caval pressures and renal and femoral arterial flows were recorded. Blood gas composition and pH and body temperature were monitored. The P/F was first determined while perfusion pressure was decreased for 2 min at each pressure by suprarenal aortic occlusion. The left renal artery in 38 of these animals was then cannulated for in situ perfusion of the kidney with blood withdrawn from a carotid artery by a Masterflex pump. The P/F was subsequently determined by changing pump flow for 2 min at each flow while recording perfusion pressure. Records were analyzed for transient and steady-state effects. Readjustments in renal vascular resistance (RVR) were apparent within 5 s after changing pressure or flow. The RVR stabilized at a new level within 2 min. Graphs of steady-state data delineated an autoregulatory range in the P/F for animals as young as 2 wk of age. We conclude that renal blood flow autoregulation in this mammal is negligible at birth and develops progressively during the first postnatal month.

Effect of protein intake on the autoregulation of renal blood flow

1990 ◽  
Vol 258 (1) ◽  
pp. F168-F174
Author(s):  
B. M. Murray ◽  
G. P. Brown
Keyword(s):  
Blood Flow ◽  
Renal Blood Flow ◽  
Carotid Arteries ◽  
Perfusion Pressure ◽  
Renal Perfusion ◽  
Cyclooxygenase Inhibitors ◽  
Base Line ◽  
Sprague Dawley ◽  
Low Protein ◽  
Sprague Dawley Rats

Autoregulatory ability was evaluated in male Sprague-Dawley rats (200-250 g) fed either low protein (LP, 6%), high protein (HP, 50%), or standard rat chow (CON) for 2 wk. Renal perfusion pressure (RPP) was first raised above normal by bilateral ligation of the carotid arteries. LP rats exhibited normal autoregulatory behavior between 130 and 100 mmHg, whereas autoregulation in HP rats was impaired (autoregulation factor 100-130; HP 0.86 +/- 0.16, LP 0.38 +/- 0.07, and CON 0.39 +/- 0.04). Autoregulation studies were repeated in HP- and LP-fed rats after administration of the cyclooxygenase inhibitors, meclofenamate and piroxicam. Cyclooxygenase inhibition did not significantly affect base-line hemodynamics but did restore the ability of the HP rat to autoregulate renal blood flow (RBF) at high RPP. (Autoregulation factor between 100 and 130 mmHg; HP 0.29 +/- 0.10, LP 0.19 +/- 0.07, P, NS). Thus an HP diet resulted in impaired autoregulation of RBF at high RPP, an effect that appears to be mediated by excessive production of vasodilatory prostaglandins.

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.

Inhibition by Bradykinin of the Vascular Effects of Pressor Hormones in the Canine Kidney: Relationship to Prostaglandins

1980 ◽  
Vol 59 (s6) ◽  
pp. 145s-148s ◽  
Author(s):  
H. Sušić ◽  
A. Nasjletti ◽  
K. U. Malik
Keyword(s):  
Blood Flow ◽  
Angiotensin Ii ◽  
Prostaglandin E2 ◽  
Vascular Reactivity ◽  
Sodium Pentobarbital ◽  
Vascular Effects ◽  
Arterial Infusion ◽  
Renal Vasoconstriction ◽  
Renal Vascular ◽  
Canine Kidney

1. Renal arterial injection of bolus doses of angiotensin II or noradrenaline, (0.06, 0.12 and 0.25 μg) caused renal vasoconstriction and decreased blood flow to the kidney in a dose-related manner in dogs anaesthetized by sodium pentobarbital. 2. The effect of angiotensin II and noradrenaline in lowering renal blood flow was reduced during renal arterial infusion of either bradykinin (10 ng min−1 kg−1) or prostaglandin E2 (4 ng min−1 kg−1). 3. Pretreatment of the dogs with an inhibitor of prostaglandin synthesis, sodium meclofenamate (5 mg/kg), blunted the inhibitory action of bradykinin, but not that of prostaglandin E2, on renal vascular reactivity to angiotensin II and noradrenaline. 4. These results indicate that bradykinin reduces the renal vasoconstriction induced by angiotensin II and noradrenaline in the dog by a mechanism dependent upon synthesis of prostaglandins.

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