Glycerol-induced Acute Renal Failure Research Articles

Neurohypophyseal vasopressor principle: vasopressor hormone as well as antidiuretic hormone?

Studies on the vasopressor role of the antidiuretic hormone arginine-vasopressin (AVP) in DOC hypertension, in two-kidney Goldblatt hypertension, and in spontaneous hypertension of rats, and during acute blood pressure elevation after intracerebroventricular injection of angiotensin II and in glycerol-induced acute renal failure of rats are reviewed. For the measurement of plasma AVP a radioimmunoassay has been developed. For this assay, a series of criteria has been met which allows the conclusion that, in plasma of rats, the antibody measures AVP only. For the blockade of vasopressor effects of AVP a specific antiserum has been used. On the basis of a series of control studies it has been concluded, but not proven that the antiserum lowers blood pressure exclusively by blockade of AVP. It could be shown that in the various animal models of hypertension and of acute blood pressure elevation AVP exerts systemic vasoconstriction when its plasma concentrations are elevated. In those models where the renin-angiotensin system played no role in blood pressure control, the height of blood pressure was closely related to the plasma AVP concentrations. When this relationship was compared with that obtained after the i.v. infusion or injection of AVP, a marked shift to the left became apparent. Hence, sensitization to the vasopressor effect of AVP had occurred, the factor of sensitization amounting to more than 1,000. It is concluded that AVP is not only an antidiuretic hormone but also a vasopressor hormone, and that any systemic vasopressor effect of AVP requires a mechanism of sensitization.

Vasopressin and renin in glycerol-induced acute renal failure in the rat.

HomeCirculation ResearchVol. 41, No. 4Vasopressin and renin in glycerol-induced acute renal failure in the rat. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBVasopressin and renin in glycerol-induced acute renal failure in the rat. K G Hofbauer, A Konrads, K Bauereiss, B Möhring, J Möhring and F Gross K G HofbauerK G Hofbauer Search for more papers by this author , A KonradsA Konrads Search for more papers by this author , K BauereissK Bauereiss Search for more papers by this author , B MöhringB Möhring Search for more papers by this author , J MöhringJ Möhring Search for more papers by this author and F GrossF Gross Search for more papers by this author Originally published1 Oct 1977https://doi.org/10.1161/01.RES.41.4.424Circulation Research. 1977;41:424–428 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Fabris A and Fabris G (1995) Rhabdomyolysis and Acute Renal Failure Acute Renal Failure in the Critically Ill, 10.1007/978-3-642-79244-1_9, (165-177), . Hura C and Stein J (1992) Renal Blood Flow Comprehensive Physiology, 10.1002/cphy.cp080125, (1129-1184), Online publication date: 1-Dec-1992. Curry S, Chang D and Connor D (1989) Drug- and toxin-induced rhabdomyolysis, Annals of Emergency Medicine, 10.1016/S0196-0644(89)80933-3, 18:10, (1068-1084), Online publication date: 1-Oct-1989. Honda N, Hishida A, Ikuma K and Yonemura K (1987) Acquired resistance to acute renal failure, Kidney International, 10.1038/ki.1987.136, 31:6, (1233-1238), Online publication date: 1-Jun-1987. Cowley A and Liard J (1987) Cardiovascular Actions of Vasopressin Vasopressin, 10.1007/978-1-4615-8129-1_10, (389-433), . Ikuma K, Honda N, Hishida A and Nagase M (1986) Loss of glomerular responses to vasoconstrictor agents in rabbits recovering from ARF, Kidney International, 10.1038/ki.1986.263, 30:6, (836-841), Online publication date: 1-Dec-1986. Krakoff L, Elijovich F and Barry C (1985) The Role of Vasopressin in Experimental and Clinical Hypertension, American Journal of Kidney Diseases, 10.1016/S0272-6386(85)80064-0, 5:4, (A40-A47), Online publication date: 1-Apr-1985. Rascher W, Lang R and Unger T (1985) Vasopressin, Cardiovascular Regulation, and Hypertension Neurobiology of Vasopressin, 10.1007/978-3-642-68493-7_4, (101-136), . Andreucci V (1984) Pathophysiology of Ischemic/ Toxic Acute Renal Failure Acute Renal Failure, 10.1007/978-1-4613-2841-4_1, (1-50), . Fried T and Stein J (1984) Experimental Acute Renal Failure: Pathophysiology and Methods of Protection Nephrology, 10.1007/978-1-4612-5284-9_65, (731-747), . Kokot F (1984) Endocrine System in Acute Renal Failure Acute Renal Failure, 10.1007/978-1-4613-2841-4_5, (167-175), . Seybold D and Gessler U (1984) Die Niere im Schock und Schockniere — Nosologie, Pathophysiologie, Klinik und Therapie Schock, 10.1007/978-3-642-82076-2_6, (261-321), . Honda P and Kurokawa G (1983) Acute renal failure and rhabdomyolysis, Kidney International, 10.1038/ki.1983.112, 23:6, (888-898), Online publication date: 1-Jun-1983. Aisenbrey G and Berl T (2006) ROLE OF VASOPRESSEN IN THE CONTROL OF SYSTEMIC HEMODYNAMICS-LESSONS LEARNED FROM THE BRATTLEBORO RAT, Annals of the New York Academy of Sciences, 10.1111/j.1749-6632.1982.tb37441.x, 394:1, (299-308) Smolens P and Stein J (1981) Pathophysiology of acute renal failure, The American Journal of Medicine, 10.1016/0002-9343(81)90568-4, 70:3, (479-482), Online publication date: 1-Mar-1981. Andrews C and Brenner B (1981) Relative contributions of arginine vasopressin and angiotensin II to maintenance of systemic arterial pressure in the anesthetized water-deprived rat., Circulation Research, 48:2, (254-258), Online publication date: 1-Feb-1981. Solez K, Ideura T, Silvia C, Hamilton B and Saito H (1980) Clonidine after renal ischemia to lessen acute renal failure and microvascular damage, Kidney International, 10.1038/ki.1980.141, 18:3, (309-322), Online publication date: 1-Sep-1980. Mendelsohn F and Smith E (1980) Intrarenal renin, angiotensin II, and plasma renin in rats with uranyl nitrate-induced and glycerol-induced acute renal failure, Kidney International, 10.1038/ki.1980.54, 17:4, (465-472), Online publication date: 1-Apr-1980. Mason J, Kain H, Shiigai T, Welsch J, Schlecker H and Steff M (1979) The early phase of experimental acute renal failure, Pfl�gers Archiv European Journal of Physiology, 10.1007/BF00582902, 380:3, (233-243), . Konrads A, Hofbauer K, Werner U and Gross F (1978) Effects of vasopressin and its deamino-d-arginine analogue on renin release in the isolated perfused rat kidney, Pfl�gers Archiv European Journal of Physiology, 10.1007/BF00584378, 377:1, (81-85), Online publication date: 1-Oct-1978. Haack D and M�hring J (1978) Vasopressin-mediated blood pressure response to intraventricular injection of angiotensin II in the rat, Pfl�gers Archiv European Journal of Physiology, 10.1007/BF00584856, 373:2, (167-173), Online publication date: 1-Feb-1978. M�hring J (1978) Neurohypophyseal vasopressor principle: Vasopressor hormone as well as antidiuretic hormone?Das vasopressorische Prinzip der Neurohypophyse: Ist es nicht nur das antidiuretische Hormon, sondern auch ein vasopressorisches Hormon?, Klinische Wochenschrift, 10.1007/BF01477456, 56:S1, (71-79), Online publication date: 1-Jan-1978. Möhring J, Möhring B, Petri M and Haack D (1978) Plasma vasopressin concentrations and effects of vasopressin antiserum on blood pressure in rats with malignant two-kidney Goldblatt hypertension., Circulation Research, 42:1, (17-22), Online publication date: 1-Jan-1978. October 1, 1977Vol 41, Issue 4 Advertisement Article InformationMetrics Copyright © 1977 by American Heart Associationhttps://doi.org/10.1161/01.RES.41.4.424 Originally publishedOctober 1, 1977 PDF download Advertisement

Glycerol-induced acute renal failure in the two kidney Goldblatt rat.

One to four weeks after the left renal artery was clipped and the contralateral kidney was left untouched in Sprague-Dawley rats (two-kidney Goldblatt preparation), the clips were removed under ether anesthesia and 10 ml/kg body wt of either 150 mM NaCl (control) or 50% glycerol in water (experimental) were injected intramuscularly. The next day the rats were anesthetized (sodium pentobarbital) and the renal function of both kidneys was measured, after which the renal cortical renin content was measured by incubation of tissue homogenate with angiotensinase-free rat renin substrate. Radioimmunoassay was used to determine the rate of angiotensin I production. Compared with controls, both kidneys of glycerol-injected rats had reduced GFR (left 28, right 18% of controls), increased percentage of fractional water excretion (left 5, right 6 times controls), and increased percentage of fractional Na excretion (left 3, right 4 times controls). Despite large differences in renal renin (left 28, 676, right 1,329 ng angiotensin I/h per mg protein), the extent of renal failure produced by glycerol was equal in the left and right kidneys. These results are inconsistent with the hypothesis that renal renin content is directly related to the severity of glycerol-induced renal failure in rats.

Renal blood flow, afferent vascular resistance, and estimated glomerular capillary pressure in the nonexposed rat kidney.

HomeCirculation ResearchVol. 41, No. 1Renal blood flow, afferent vascular resistance, and estimated glomerular capillary pressure in the nonexposed rat kidney. Free AccessAbstractPDF/EPUBAboutView PDFSections ToolsAdd to favoritesDownload citationsTrack citationsPermissions ShareShare onFacebookTwitterLinked InMendeleyReddit Jump toFree AccessAbstractPDF/EPUBRenal blood flow, afferent vascular resistance, and estimated glomerular capillary pressure in the nonexposed rat kidney. I Ishikawa and N K Hollenberg I IshikawaI Ishikawa Search for more papers by this author and N K HollenbergN K Hollenberg Search for more papers by this author Originally published1 Jul 1977https://doi.org/10.1161/01.RES.41.1.67Circulation Research. 1977;41:67–73 Previous Back to top Next FiguresReferencesRelatedDetailsCited By Yu M, Kim J, Lee S, Choi J, Kim Y, Han S, Lee H, Cha R, Lee J, Lee J, Kim D, Kim Y and Yang S (2020) Krüppel-like factor 15 is a key suppressor of podocyte fibrosis under rotational force-driven pressure, Experimental Cell Research, 10.1016/j.yexcr.2019.111706, 386:1, (111706), Online publication date: 1-Jan-2020. Ishikawa I, Shikura N and Takada K (2009) Amelioration of Glycerol-Induced Acute Renal Failure in Rats by an Adenosine A 1 Receptor Antagonist (FR-113453) , Renal Failure, 10.3109/08860229309065565, 15:1, (1-5), Online publication date: 1-Jan-1993. Steinhausen M, Endlich K and Wiegman D (1990) Glomerular blood flow, Kidney International, 10.1038/ki.1990.271, 38:5, (769-784), Online publication date: 1-Nov-1990. Sossenheimer M, Fleming J and Steinhausen M (1987) Passage of microspheres through vessels of normal and split hydronephrotic rat kidneys, American Journal of Anatomy, 10.1002/aja.1001800208, 180:2, (185-194), Online publication date: 1-Oct-1987. TYSSEBOTN I and KIRKEBØ A (1979) Renal cortical blood flow distribution measured by hydrogen clearance during dopamine and acetylcholine infusion. Effect of electrode thickness and position in cortex, Acta Physiologica Scandinavica, 10.1111/j.1748-1716.1979.tb06418.x, 106:4, (385-393), Online publication date: 1-Aug-1979. Hsu C, Kurtz T and Sands C (1979) Intrarenal vascular resistance in glycerol-induced acute renal failure in the rat., Circulation Research, 45:5, (583-587), Online publication date: 1-Nov-1979. July 1, 1977Vol 41, Issue 1 Advertisement Article InformationMetrics Copyright © 1977 by American Heart Associationhttps://doi.org/10.1161/01.RES.41.1.67 Originally publishedJuly 1, 1977 PDF download Advertisement

Cardiac output and renal blood flow in glycerol-induced acute renal failure in the rat.

Cardiac output (CO) and renal blood flow (RBF) were simultaneously evaluated by the microsphere method in water-drinking and chronic saline-drinking rats at 3, 12 and 24 hours after induction of acute renal failure by glycerol injection. Threee hours after glycerol injection CO and RBF decreased to 36% and 20% of the respective controls in water-drinking rats and to 41% and 24% of the controls in saline-drinking rats. Renal vascular resistance (RVR) increased significantly in both groups at this time. Isoncotic plasma expansion (3% of body weight) restored the RBF and RVR to normal in water-drinking rats 3 hours post-glycerol injection, althought CO increased to only 70% of the control. Twelve hours after glycerol injection, CO and RBF returned to normal in saline-drinking rats, whereas they remained lower than controls in water-drinking rats. Twenty-four hours post-glycerol injection, when acute renal failure was evident as indicated by blood urea nitrogen (BUN) values of 116.9 and 63.8 mg/100 ml in water- and saline-drinking rats, respectively, CO and RBF returned to normal, except that the CO of of water-drinking rats was slightly higher than control. Thus, we conclude that decreased CO is an important determinant of the early decrease in renal perfusion in glycerol-induced acute renal failure. Furthermore, the observed earlier return of CO and RBF to normal in saline-drinking rats may be partly responsible for reproducing the severity of acute renal failure.

Action of the competitive angiotensin II antagonist saralasin during the initial phase of glycerol-induced acute renal failure of the rat.

The effects of the competitive angiotensin II antagonist saralasin (1-sarcosine-8-alanine-5-isoleucine-angiotensin II) on renal function in healthy rats and in rats with myohemoglobinuric acute renal failure were studied. Acute renal failure was induced by an intramuscular injection of 50% glycerol (10 ml.kg-1). Functional impairment of the glycerol treated animals consisted in a decrease of renal blood flow (electromagnetic flowmeter) and GFR and in an increase of urine volume and arterial blood pressure. In healthy rats saralasin (6 microgram.kg-1.min-1 i.v.) had no renal effects by itself but antagonized the angiotensin II (200 ng.kg-1.min i.v.) induced fall of renal blood flow and GFR and the increase of arterial blood pressure. Given to glycerol treated animals saralasin did not induce any change of arterial blood pressure, renal blood flow, GFR or the urinary excretion of fluid and sodium.

Renal cortical blood flow in glycerol-induced acute renal failure in the rat.

Renal hemodynamics and renal function were evaluated in rats at 3, 24, and 48 hours and at 7 days after the induction of acute renal failure (ARF) by glycerol injection. Three hours after induction of ARF, creatinine clearance was 0.04 ml/min/100 g; renal blood flow (RBF), 1.99 ml/min/100 g; and filtration fraction, 3.7%. All were abnormally low. Although the administration of isotonic saline (total dose, 3% of body weight) to rats 3 hours after glycerol injection significantly improved creatinine clearance (0.17 ml/min/100 g), RBF (2.54 ml/min/100 g), and filtration fraction (12.9%), these values still were significantly lower than those of controls (creatinine clearance = 0.50 ml. ml/min/100 g, RBF = 4.92 ml/min/100 g, filtration fraction = 20.0%, all P values less than 0.001). Serum creatinine concentrations were significantly elevated at 24 hours (3.72% gm/100 ml), 48 hours (4.69 mg/100 ml), and 7 days (0.66 mg/100 ml) after glycerol injection compared to control (0.46 mg/100 ml, all P less than 0.01). RBF during these phases was not different from normal (4.41 ml/min/100 g). RBF 3 hours after bilateral ureteral obstruction was measured to determine the effects of tubular obstruction on renal hemodynamics. The RBF of rats with ureteral obstruction (4.12 ml/min/100 g) was not significantly different from controls (4.41 ml/min/100 g), suggesting that tubular obstruction in this model of ARF is probably not the cause of decreased RBF. The depressed glomerular filtration, as reflected by the decreased creatinine clearance that occurs during glycerol-induced ARF, is probably related to altered intrarenal vascular resistance or to changes in glomerular capillary permeability, or both.

Effect of dose on renal diatrizoate concentrations in experimental acute renal failure.

In rats with glycerol-induced acute renal failure (ARF) and controls, renal concentrations of 125I-labelled sodium diatrizoate were measured 5 min after intravenous doses ranging from 14 to 1,800 mg/kg body weight. Renal concentrations of diatrizoate, at all doses, were much higher in controls than in ARF. A linear relationship existed between dose and renal concentration in ARF. In controls, at doses above 225 mg/kg body weight, the fraction of the dose present in the kidneys diminished and renal iodine content approached that observed in ARF. Differences in diatrizoate concentration which existed between cortical and medullary zones in healthy kidneys at low dises were progressively eliminated as dosage increased, consistent with the osmatic fiutryiv rggrvy of diatrizoate. In ARF, the pattern of intrarenal distribution at all doses was similar to that seen in controls at high doses, though concentrations in outer cortex were consistently slightly higher than those in inner cortex. These observations suggest continuing though reduced, filtration of diatrizoate in ARF by glomeruli already subjected to a large solute load.

Indomethacin enhancement of glycerol-induced acute renal failure in rabbits

Seventy-three rabbits (2 to 3 kg in weight) were studied during a control period and after receiving 50% glycerol (G) or mercuric chloride (M) with or without indomethacin (I) (controls received the diluent used for I). Plasma creatinine, plasma renin activity, blood pressure, sodium and potassium concentrations, hematocrit value, urinary output, body wt and histologic appearance of the kidney were determined. I enhanced the incidence and severity of the acute renal failure produced by G but failed to aggravate that produced by M. Because the dose of I used in this study blocked the synthesis of renal prostaglandins in the rabbit, we suggest that renal prostaglandins protect against the development of G-induced acute renal failure (a circulatory type of renal failure) in this animal model. Furthermore, the failure of I to aggravate M-induced acute renal failure indicates that it is unlikely that I aggravates G-induced acute renal failure by a direct nephrotoxic effect. No evidence was found for other possible side actions of I being responsible for the observed aggravation.

Resistance to acute renal failure afforded by prior renal failure: examination of the role of renal renin content.

In this study, rats recovering from glycerol-induced acute renal failure were found to be protected from mercury-induced nephropathy, and HgCl2 poisoning protected rats from developing myohemoglobinuric renal failure. In view of the widely disparate nature of the renal failure models used, refractoriness appears to relate to an altered sensitivity of the organism itself rather than reflecting resistance to a particular nephropathic challenge. Renal renin content of the rats at the time of rechallenge was normal or high, a finding which contrasts sharply with that of chronically saline-loaded animals which also are refractory to ARF but have a maximally suppressed renal renin content. Renal renin depletion is not essential to the prevention of acute renal failure in the rat.

Endogenous prostaglandins and osmotic water flow in the toad bladder.

Endogenous prostaglandins and osmotic water flow in the toad bladder.

Intrarenal hemodynamics in glycerol-induced myohemoglobinuric acute renal failure in the rat.

A modified 138 Xe washout technique was used to study changes in intrarenal hemodynamics during glycerol-induced acute renal failure in the rat. Within 10 minutes after glycerol injection, the flow fraction supplied to component 1 of the washout curve ("cortex A") decreases, reaching minimum values 24 hours afer glycerol (31% of control conditions). Seven days thereafter five of the rats, still uremic, showed cortical flow fractions less than 50% of control values. Nine others had recovered. Twenty-four hours after glycerol, renal blood flow was 27% and increased to 86% of control conditions in the recovered rats 7 days after glycerol. 85 Kr autoradiographs and silicone rubber casts of the renal vasculature demonstrated a severe cortical hypoperfusion at the height of oliguria that gradually disappeared in parallel with the functional recovery of the kidney. These observations, in good agreement with micropuncture data, suggest that oliguria and renal insufficiency in this experimental model are the result of a primary decrease in glomerular filtration rate due to an increased preglomerular resistance.

Effects of ureteral pressure elevation on renal hemodynamics and urine concentration.

ARTICLESEffects of ureteral pressure elevation on renal hemodynamics and urine concentrationWN Suki, AG Guthrie, M Martinez-Maldonado, and G EknoyanWN Suki, AG Guthrie, M Martinez-Maldonado, and G EknoyanPublished Online:01 Jan 1971https://doi.org/10.1152/ajplegacy.1971.220.1.38MoreSectionsPDF (1 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Next Download PDF FiguresReferencesRelatedInformation Cited ByGlomerular hyperpermeability after acute unilateral ureteral obstruction: effects of Tempol, NOS, RhoA, and Rac-1 inhibitionJulia Dolinina, Anna Rippe, Peter Bentzer, and Carl M. Öberg22 August 2018 | American Journal of Physiology-Renal Physiology, Vol. 315, No. 3Obstructive UropathyPartial unilateral ureteral obstruction in rats27 March 2002 | Neurourology and Urodynamics, Vol. 21, No. 3Physiopathologie de la colique néphrétique. Retentissement rénalRéanimation Urgences, Vol. 8, No. 7Obstructive Nephropathy in the pig Aspects of renal hemodynamics and hormonal changes during acute unilateral ureteral obstruction12 October 2011 | APMIS, Vol. 106, No. S82Intrapelvic pressure monitoring in the partially obstructed porcine kidneyUrology, Vol. 44, No. 4Regulation of the renal angiotensin II receptor gene in acute unilateral ureteral obstructionKidney International, Vol. 45, No. 6Regulation of renin-angiotensin system in unilateral ureteral obstructionKidney International, Vol. 44, No. 2The Pathophysiology of Ureteral ObstructionJournal of Endourology, Vol. 7, No. 2First-pass evaluation of renal perfusion with turboflash MR imaging and superparamagnetic iron oxide particlesJournal of Magnetic Resonance Imaging, Vol. 3, No. 1A New Test to Predict Reversibility of Hydronephrotic Atrophy After Stable Partial Unilateral Ureteral ObstructionJournal of Urology, Vol. 140, No. 6The effect of radiopharmaceutical choice on the assessment of the relative renal function in upper urinary tract obstructionEuropean Journal of Nuclear Medicine, Vol. 14, No. 1Pathophysiology of obstructive nephropathyWorld Journal of Urology, Vol. 6, No. 1Role of angiotensin II in renal hemodynamic functions during the initial stages of acute ureteral obstructionLife Sciences, Vol. 42, No. 20Disorders of Glomerular FiltrationGlomerular Filtration Response to Acute Ureteral Obstruction in the DogJournal of Urology, Vol. 134, No. 5Intensive-care AuditThe Lancet, Vol. 325, No. 8443RECOVERY AFTER RELIEF OF RENAL OBSTRUCTIONThe Lancet, Vol. 325, No. 8443Acute Obstructive Renal Failure (Postrenal Failure)Use of hydrogen gas clearance for measurement of renal circulationUrology, Vol. 22, No. 5Impact of age on effects of ureteral obstruction on renal functionKidney International, Vol. 24, No. 5Reversibility of Preglomerular Active Vasoconstriction in the First Weeks after Complete Unilateral Ureteral Obstruction by Inhibition of Prostaglandin SynthesisJournal of Urology, Vol. 130, No. 4Pathophysiology of obstructive nephropathyKidney International, Vol. 23, No. 2Acute Olifuric Interstitia NephritisChanges in glomerular filtration rate during complete ureteral obstruction in ratsKidney International, Vol. 19, No. 4Pathophysiology of obstructive nephropathyKidney International, Vol. 18, No. 3Acute oliguric interstitial nephritisKidney International, Vol. 16, No. 6Excretion of Sodium and Methylglucamine Diatrizoate after Longtime Unilateral Ureteric Stasis in the Rabbit5 November 2016 | Acta Radiologica. Diagnosis, Vol. 20, No. 1AProstaglandin-mediated hyperemia and renin-mediated hypertension during acute ureteral obstructionProstaglandins, Vol. 16, No. 6Urine concentration and dilution in the rat: Contribution of papillary structures during high rates of urine flowKidney International, Vol. 13, No. 3Effects of acute ureteral obstruction on glomerular hemodynamics in rat kidneyKidney International, Vol. 12, No. 6Insufficienza Renale Cronica Da Affezione Urologica Misconosciuta: Uropatia Ostruttiva13 November 2018 | Urologia Journal, Vol. 44, No. 4Mechanism of renin release during acute ureteral constriction in dogs.Circulation Research, Vol. 40, No. 3Prostaglandins, a Link between Renal Hydro- and Hemodynamic in DogsActa Physiologica Scandinavica, Vol. 97, No. 3Obstructive polyuric renal failure following renal transplantationThe American Journal of Medicine, Vol. 60, No. 5Renal cortical blood flow in glycerol-induced acute renal failure in the rat.Circulation Research, Vol. 38, No. 1Glomerular filtration response to elevated ureteral pressure in both the hydropenic and the plasma-expanded rat.Circulation Research, Vol. 37, No. 6Blood urea nitrogen and serum creatinineUrology, Vol. 5, No. 5Renal function after release of chronic unilateral hydronephrosis in manKidney International, Vol. 7, No. 3Whole kidney volume/pressure relationshipsKidney International, Vol. 7, No. 1Renal Function in Experimental Chronic Hydronephrosis: II. Backflow Studies with Radionuclides21 March 2011 | Scandinavian Journal of Urology and Nephrology, Vol. 9, No. 3Régénération du rein après levée d'une occlusion de l'uretère chez le ratKidney International, Vol. 5, No. 3Experimental Ureteric ObstructionBritish Journal of Urology, Vol. 46, No. 1Nierengewebsspiegelbestimmung von AntibiotikaInfection, Vol. 1, No. 4Renal Function during Acute Total Ureteral Occlusion and the Role of the Lymphatics: An Experimental Study in DogsJournal of Urology, Vol. 109, No. 3 More from this issue > Volume 220Issue 1January 1971Pages 38-43 Copyright & PermissionsCopyright © 1971 by American Physiological Societyhttps://doi.org/10.1152/ajplegacy.1971.220.1.38PubMed5538669History Published online 1 January 1971 Published in print 1 January 1971 Metrics

The Prevention of Acute Renal Failure in the Rat by Long-Term Saline Loading: A Possible Role of the Renin-Angiotensin Axis

SummarySubstitution of 1% saline for drinking water largely prevents the development of established acute renal failure in rats given glycerol intramuscularly. Control experiments indicate that this protection from acute renal failure is not due to the blood volume expansion, polyuria, polydypsia, lower urine osmolality, or other parameters studied. It is suggested that the depletion of renin, associated with chronic saline-loading, may have played a protective role, and that the renin-angiotensin axis may be a potent factor in the development of glycerol-induced acute renal failure in the rat.