Renal Vasoconstriction in Glycerol-Induced Acute Renal Failure. Studies in the Isolated Perfused Rat Kidney

1978 ◽  
Vol 55 (3) ◽  
pp. 249-252
Author(s):  
K. G. Hofbauer ◽  
K. Bauereiss ◽  
A. Konrads ◽  
F. Gross
Keyword(s):  
Renal Failure ◽  
Acute Renal Failure ◽  
Vascular Resistance ◽  
Rat Kidney ◽  
Renal Vascular Resistance ◽  
Renin Release ◽  
Pass System ◽  
Renal Vasoconstriction ◽  
Renal Vascular

1. Acute renal failure was produced in rats by the intramuscular injection of glycerol (6.1 mol/l, 10 ml/kg). Either 2 or 4–6 h later the right kidney was isolated and perfused for 1 h with an electrolyte solution containing a gelatin preparation (Haemaccel, 35 g/l) at pressures between 90 and 100 mmHg in a single-pass system. 2. In kidneys taken from rats with acute renal failure renal vascular resistance was markedly increased immediately after the start of the perfusion as compared with control kidneys taken from untreated rats. During the following 30 min of perfusion the resistance progressively decreased and, at 1 h of perfusion, was similar to that in control kidneys or only moderately elevated. 3. Despite the reduction of renal vascular resistance glomerular filtration rate was still markedly impaired after 1 h of perfusion and fractional reabsorption of sodium and water as well as the secretion of p-aminohippurate were diminished. Renal venous renin concentration and renin release were lower in kidneys taken from rats with acute renal failure than in the control experiments. 4. These results suggest that the increase in renal vascular resistance and the stimulation of renin release after injection of glycerol in vivo are the consequence of extra-rather than intra-renal mechanisms.

Glycerol-Induced Acute Renal Failure in Brattleboro Rats with Hypothalamic Diabetes Insipidus

1979 ◽  
Vol 56 (2) ◽  
pp. 133-138 ◽  
Author(s):  
A. Konrads ◽  
K. G. Hofbauer ◽  
K. Bauereiss ◽  
J. Möhring ◽  
F. Gross
Keyword(s):  
Blood Pressure ◽  
Renal Failure ◽  
Acute Renal Failure ◽  
Diabetes Insipidus ◽  
Vascular Resistance ◽  
Plasma Renin ◽  
Renal Vascular Resistance ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Renal Vascular

1. During the development of glycerol-induced acute renal failure in Sprague-Dawley rats, plasma concentrations of vasopressin rise and probably induce an increase in blood pressure. 2. In the present studies the role of vasopressin in acute renal failure was further analysed by experiments in Brattleboro rats homozygous for hereditary hypothalamic diabetes insipidus which were injected intramuscularly with 10 ml of glycerol/kg (61 mmol/l). 3. After the injection of glycerol plasma osmolality increased transiently and packed cell volume was elevated. The rats became anuric and plasma urea concentrations rose progressively. Plasma renin concentration increased significantly within 2 h. Plasma renin substrate concentration rose progressively and had almost doubled by 8 h. 4. In contrast with previous observations in Sprague-Dawley rats, blood pressure did not rise in rats with diabetes insipidus after the injection of glycerol. 5. When 2 h after the injection of glycerol kidneys were taken from rats with diabetes insipidus and perfused with an electrolyte solution in a single-pass system for 1 h, renal vascular resistance was 30% higher than in control kidneys 10 min after the start of the perfusion and remained elevated thereafter. In similar experiments with kidneys from Sprague-Dawley rats with acute renal failure, renal vascular resistance was increased fivefold immediately after the start of the perfusion, but decreased subsequently. 6. These data support the idea that in glycerol-induced acute renal failure of Sprague-Dawley rats an increased release of vasopressin is responsible for the elevation of blood pressure and suggest that this hormone also participates in renal vasoconstriction. However, a rise of plasma vasopressin concentrations alone cannot fully explain the increase in renal vascular resistance and the development of acute renal failure.

Inhibition by bradykinin of renal adrenergic effects in anesthetized rats

1984 ◽  
Vol 246 (4) ◽  
pp. F387-F394
Author(s):  
K. Inokuchi ◽  
K. U. Malik
Keyword(s):  
Arachidonic Acid ◽  
Renal Artery ◽  
Vascular Resistance ◽  
Nerve Stimulation ◽  
Rat Kidney ◽  
Renal Vascular Resistance ◽  
Cyclooxygenase Inhibitors ◽  
Renal Nerve ◽  
Anesthetized Rats ◽  
Renal Vascular

We studied the contribution of prostaglandins to the actions of bradykinin at the renal vascular adrenergic neuroeffector junction by examining the effect of the peptide on the decrease in renal blood flow elicited by renal nerve stimulation and injected norepinephrine in pentobarbital-anesthetized rats with or without pretreatment with the cyclooxygenase inhibitors sodium meclofenamate or indomethacin. Infusion of bradykinin, 10 ng X kg-1 X min-1, into the renal artery reduced both the basal and the rise in renal vascular resistance produced by nerve stimulation or norepinephrine. The prostaglandin precursor arachidonic acid, 5 micrograms X kg-1 X min-1, infused into the renal artery, also reduced renal vascular resistance and the vasoconstrictor response elicited by either adrenergic stimulus. In animals pretreated with either sodium meclofenamate or indomethacin, the effect of arachidonic acid, but not that of bradykinin, to produce renal vasodilation and to attenuate adrenergically induced renal vasoconstriction was abolished. These data suggest that bradykinin produces renal vasodilation and inhibits the renal vasoconstrictor effect of adrenergic stimuli in the rat kidney in vivo by a mechanism unrelated to prostaglandin synthesis.

Acetylcholine chloride and renal hemodynamics during postnatal maturation in conscious lambs

1999 ◽  
Vol 87 (4) ◽  
pp. 1296-1300 ◽  
Author(s):  
Alp Sener ◽  
Francine G. Smith
Keyword(s):  
Renal Artery ◽  
Vascular Resistance ◽  
Renal Hemodynamics ◽  
Renal Vascular Resistance ◽  
Postnatal Maturation ◽  
Renal Vasoconstriction ◽  
Acetylcholine Chloride ◽  
Renal Vascular ◽  
Dose Dependent ◽  
Conscious Animals

To test the hypothesis that acetylcholine-induced relaxation of the renal artery decreases with postnatal age, we measured parameters of renal hemodynamics before and for 35 s after aortic suprarenal injection of acetylcholine in conscious, chronically instrumented lambs aged ∼1 wk ( n = 5) and ∼6 wk ( n = 5). Acetylcholine was administered in one of five doses ranging from 0 to 10 mg/kg body wt; doses were administered randomly, in the same volume. There were significant age- and dose-dependent changes in renal vascular resistance after acetylcholine administration, such that the response was greater in 1-wk-old lambs. After the highest dose tested, renal vascular resistance decreased by 13.6 ± 7.3 (SD) mmHg ⋅ ml−1 ⋅ min ⋅ g kidney wt in 1-wk-old lambs and by 9.1 ± 3.2 mmHg ⋅ ml−1 ⋅ min ⋅ g kidney wt in 6-wk-old lambs at 35 s. We also observed a transient renal vasoconstriction before the renal vasodilatation in 6-wk-old lambs but not in 1-wk-old animals. These data provide the first age- and dose-dependent effects of exogenous administration of acetylcholine on renal hemodynamics during maturation in conscious animals.

Inhibition of ROMK blocks macula densa tubuloglomerular feedback yet causes renal vasoconstriction in anesthetized rats

2017 ◽  
Vol 312 (6) ◽  
pp. F1120-F1127 ◽  
Author(s):  
Magali Araujo ◽  
William J. Welch ◽  
Xiaoyan Zhou ◽  
Kathleen Sullivan ◽  
Shawn Walsh ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Tubuloglomerular Feedback ◽  
Volume Depletion ◽  
Renal Vasoconstriction ◽  
Compound C ◽  
Altered Blood ◽  
Renal Vascular ◽  
Dose Dependent

The Na+-K+-2Cl− cotransporter (NKCC2) on the loop of Henle is the site of action of furosemide. Because outer medullary potassium channel (ROMK) inhibitors prevent reabsorption by NKCC2, we tested the hypothesis that ROMK inhibition with a novel selective ROMK inhibitor (compound C) blocks tubuloglomerular feedback (TGF) and reduces vascular resistance. Loop perfusion of either ROMK inhibitor or furosemide caused dose-dependent blunting of TGF, but the response to furosemide was 10-fold more sensitive (IC50 = 10−6 M for furosemide and IC50 = 10−5 M for compound C). During systemic infusion, both diuretics inhibited TGF, but ROMK inhibitor was 10-fold more sensitive (compound C: 63% inhibition; furosemide: 32% inhibition). Despite blockade of TGF, 1 h of constant systemic infusion of both diuretics reduced the glomerular filtration rate (GFR) and renal blood flow (RBF) by 40–60% and increased renal vascular resistance (RVR) by 100–200%. Neither diuretic altered blood pressure or hematocrit. Proximal tubule hydrostatic pressures (PPT) increased transiently with both diuretics (compound C: 56% increase; furosemide: 70% increase) but returned to baseline. ROMK inhibitor caused more natriuresis (3,400 vs. 1,600% increase) and calciuresis (1,200 vs. 800% increase) but less kaliuresis (33 vs. 167% increase) than furosemide. In conclusion, blockade of ROMK or Na+-K+-2Cl− transport inhibits TGF yet increases renal vascular resistance. The renal vasoconstriction was independent of volume depletion, blood pressure, TGF, or PPT.

Effect of L-arginine on myoglobin-induced acute renal failure in the rabbit

1996 ◽  
Vol 270 (5) ◽  
pp. F784-F789
Author(s):  
Y. Wakabayashi ◽  
R. Kikawada
Keyword(s):  
Nitric Oxide ◽  
Renal Failure ◽  
Blood Flow ◽  
Acute Renal Failure ◽  
Protective Effect ◽  
Potent Inhibitor ◽  
Renal Vasoconstriction ◽  
Baseline Levels ◽  
Nitrite Nitrate ◽  
Renal Vascular

Because myoglobin is a potent inhibitor of nitric oxide (NO), we tested whether myoglobin infusion results in renal vasoconstriction and dysfunction, on which L-arginine, a source of NO, has a protective effect in sedated, nondehydrated, and nonacidotic rabbits. The infusion of myoglobin (375 mg/kg) resulted in a decrease in renal blood flow, an increase in renal vascular resistance, and a decrease in creatine clearance associated with a decrease in urinary excretory rate of nitrite/nitrate and guanosine 3',5'-cyclic monophosphate (cGMP). These values 1-2 h after the infusion were significantly different from baseline levels. Co-administration of L-arginine (150 mg/kg bolus followed by 150 mg.kg(-1).min(-1) reversed these changes significantly with attenuation of urinary excretory rate of nitrite/nitrate and cGMP. This study suggests that the myoglobin-induced renal vasoconstriction and dysfunction and protective effect of L-arginine on these outcomes could be mediated through the NO system.

A renal vasodilator effect of angiotensin II revealed by dual thromboxane inhibition

1994 ◽  
Vol 72 (6) ◽  
pp. 632-636 ◽  
Author(s):  
Al-Hassan Badahman ◽  
Thomas W. Wilson
Keyword(s):  
Angiotensin Ii ◽  
Vascular Resistance ◽  
Renal Vascular Resistance ◽  
Sprague Dawley ◽  
Synthesis Inhibition ◽  
Renal Vasoconstriction ◽  
Sprague Dawley Rats ◽  
Renal Vascular ◽  
Arachidonate Release ◽  
Stimulation Of

Angiotensin II (AII) stimulates arachidonate release from renal endothelial and other ceils. Arachidonate is then metabolized by cyclooxygenase to prostaglandin (PG) H2, then PGI2 and thromboxane A2 (TXA2). PGH2 and TXA2 activate the same receptor and should augment AII-mediated vasoconstriction, whereas PGI2 is a vasodilator. We had previously shown that inhibiting TXA2 synthesis with furegrelate (FRG) redirects PGH2 metabolism toward PGI2, causing renal vasodilation. Because TXA2 synthesis inhibition may be incomplete and unmetabolized PGH2 may cause vasoconstriction, we reasoned that adding a PGH2/TXA2 receptor antagonist (BMS 180,290, formerly SQ 29548 (SQ)) to furegrelate should cause further renal vasodilation in the presence of AII Eight groups of 10 Sprague–Dawley rats received 120-min intravenous infusions of vehicle, FRG (2 mg∙kg−1 plus 2 mg∙kg−1∙h−1), SQ (2 mg∙kg−1 plus 2 mg∙kg−1∙h−1), FRG plus SQ, AII (10 ng∙kg−1∙min−1), AII plus FRG, AII plus SQ, or AII plus FRG plus SQ. Mean arterial pressure (MAP), p-[14C]aminohippurate clearance (CPAH), and [3H]insulin clearance were averaged for each rat for the final 90 min in three clearance periods. MAP did not change with any treatment. Estimating renal vascular resistance as MAP/CPAH confirmed a renal vasoconstrictor effect of this dose of AII: 58.1 ± 6.3 vs. 47.3 ± 6.8 (arbitrary units) with the vehicle (p < 0.05). FRG, SQ, or their combination did not affect renal vascular resistance, but adding FRG or SQ to AII prevented AII-mediated renal vasoconstriction. Adding both to AII caused net renal vasodilation to 24.8 ± 2.6 (p < 0.05 vs. vehicle). Inulin clearance changed in the same direction in all groups, but the changes were less marked. We conclude that stimulation of renal arachidonate release by AII combined with TXA2 synthesis inhibition and receptor antagonism results in vasodilation. This renal effect could be due to increased and unopposed renal vasodilator PG (principally PGI2) action.Key words: renal hemodynamics, angiotensin II, prostaglandins, thromboxane.

Myogenic contribution to agonist-induced renal vasoconstriction during normoxia and hypoxia

1997 ◽  
Vol 272 (4) ◽  
pp. H1945-H1951 ◽  
Author(s):  
M. R. Eichinger ◽  
J. M. Resta ◽  
B. R. Walker
Keyword(s):  
Renal Artery ◽  
Vascular Resistance ◽  
Acute Hypoxia ◽  
Renal Perfusion ◽  
Renal Vascular Resistance ◽  
Left Renal Artery ◽  
Sprague Dawley ◽  
Renal Vasoconstriction ◽  
Arterial Blood ◽  
Renal Vascular

Acute hypoxia attenuates agonist-induced constrictor and pressor responses in conscious rats, and a recent report suggests that hypoxia may also diminish myogenic reactivity in isolated, perfused rat kidneys. Thus we hypothesized that the diminished responsiveness to pressor agents during hypoxia is caused by an impairment of myogenic reactivity. Male Sprague-Dawley rats were instrumented with a pulsed Doppler flow probe on the left renal artery, an aortic vascular occluder cuff immediately above the left renal artery to control renal perfusion pressure, and catheters were inserted to measure systemic arterial blood pressure and renal arterial pressure (RAP) and for administration of agents. Animals were studied under normoxic or acute hypoxic (fractional concentration of O2 in inspired gials = 0.12) conditions and were administered phenylephrine, arginine vasopressin, or angiotensin II. To determine the myogenic (pressure-dependent) component of agonist-induced vasoconstriction, renal vascular resistance was calculated during agonist infusion with RAP uncontrolled and with RAP controlled to preinfusion levels. Significant myogenic components of agonist-induced renal vasoconstriction were evident with all pressor agents used. However, hypoxia did not attenuate agonist-induced, pressure-dependent increases in renal vascular resistance. We conclude that the reduced vasoreactivity associated with acute hypoxia is not caused by diminished myogenic reactivity.

Renin stimulation by isoproterenol and theophylline in the isolated perfused kidney

1977 ◽  
Vol 232 (3) ◽  
pp. F248-F253 ◽  
Author(s):  
R. J. Viskoper ◽  
M. H. Maxwell ◽  
A. N. Lupu ◽  
S. Rosenfeld
Keyword(s):  
Vascular Resistance ◽  
Macula Densa ◽  
Renal Vascular Resistance ◽  
Renin Release ◽  
Rabbit Kidney ◽  
Urinary Flow ◽  
Release Studies ◽  
Renal Vascular ◽  
Additional Stimulation ◽  
Ureteral Occlusion

The intrarenal mechanisms of renin release were studied in the isolated perfused rabbit kidney during stimulation by isoproterenol, 0.01 mug/kg per min, and by theophylline, 0.87 mg/kg per min. In the absence of urinary flow during the early stages of perfusion, isoproterenol caused a 17% increase of renal vein serum renin concentration (RVSRC) (P less than 0.001) without changing renal blood flow, renal vascular resistance, or serum potassium. dl-Propranolol, 2.0 mg/kg per min. abolished this isoproterenol-induced renin release. A moderate reduction in perfusion pressure prior to the infusion of isoproterenol resulted in a marked additional stimulation of renin release. Studies during and following ureteral occlusion demonstrated that theophylline stimulates renin release by decreasing renal vascular resistance, whereas the concomitant increase in sodium transport to the macula densa exerted an opposite effect. dl-Propranolol did not affect theophylline-induced renin secretion. It is concluded that single exogenous stimuli may activate more than one intrarenal mechanism simultaneously. Isoproterenol has a direct renin-stimulatory effect on intrarenal beta-adrenergic receptors that may be reinforced by baroreceptor stimulation. Theophylline stimulates renin via a baroreceptor mechanism, with simultaneous renin suppression via a sodium-macula densa effect.

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