Effects of furosemide and acetylcholine in norepinephrine induced acute renal failure

A. De Torrente, P. D. Miller, R. E. Cronin

Research output: Chapter in Book/Report/Conference proceedingChapter

Abstract

The influence of intrarenal acetylcholine (ACh) or intravenous furosemide (F) on the course of norepinephrine (NE)-induced acute renal failure (ARF) was investigated in the dog. All groups received a 40-min intrarenal infusion of NE (0.75 μg/kg per min). Group I received NE alone; group II received ACh (20 μg/min) intrarenally which was started 30 min before NE infusion and continued throughout the study; and group III received F (10 mg/kg i.v.) before NE infusion followed by a constant infusion of F (10 mg/kg per h) throughout the study. In group IV F was started immediately after completion of NE infusion. All groups were studied before, during, and 3 h after NE infusion. Urine losses were replaced with a 0.9% sodium chloride solution. Before NE, the mean glomerular filtration rate (GFR) in the infused kidney of groups I-IV was 54.1 ± 6.5, 44.2 ± 1.3, 50.2 ± 5.3, and 57.6 ± 7.3 ml/min, respectively. During NE, GFR and renal blood flow (RBF) were undetectable in the infused kidneys of all four groups. Three hours after NE GFR was 1.3 ± 1.3 in group I and 5.9 ± 4.9 ml/min in group II. In contrast, GFR in groups III and IV was 28.4 ± 5.4 and 15.40 ± 2.4 ml/min, respectively (P < 0.01 compared to group I). Before the NE infusion RBF was comparably and significantly increased from control in groups II and III. However, osmolar clearance C(osM) was increased before NE most profoundly in group III (9.04 ± 1.25 ml/min, P < 0.01 compared to groups I and II). In group IV, C(osM) increased to 7.13 ± 1.37 ml/min (P < 0.01 compared to group I). We conclude that F exerts a significant protective effect in this ischemic model of ARF, which could not be mimicked by ACh despite comparable increases in RBF. The higher C(osM) with F may be an important intratubular factor in the protection.

Original languageEnglish (US)
Title of host publicationAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume4
Edition2
StatePublished - 1978

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Furosemide
Acute Kidney Injury
Acetylcholine
Norepinephrine
Glomerular Filtration Rate
Renal Circulation
Kidney
Sodium Chloride
Urine
Dogs

ASJC Scopus subject areas

  • Medicine(all)

Cite this

De Torrente, A., Miller, P. D., & Cronin, R. E. (1978). Effects of furosemide and acetylcholine in norepinephrine induced acute renal failure. In American Journal of Physiology - Renal Fluid and Electrolyte Physiology (2 ed., Vol. 4)

Effects of furosemide and acetylcholine in norepinephrine induced acute renal failure. / De Torrente, A.; Miller, P. D.; Cronin, R. E.

American Journal of Physiology - Renal Fluid and Electrolyte Physiology. Vol. 4 2. ed. 1978.

Research output: Chapter in Book/Report/Conference proceedingChapter

De Torrente, A, Miller, PD & Cronin, RE 1978, Effects of furosemide and acetylcholine in norepinephrine induced acute renal failure. in American Journal of Physiology - Renal Fluid and Electrolyte Physiology. 2 edn, vol. 4.
De Torrente A, Miller PD, Cronin RE. Effects of furosemide and acetylcholine in norepinephrine induced acute renal failure. In American Journal of Physiology - Renal Fluid and Electrolyte Physiology. 2 ed. Vol. 4. 1978
De Torrente, A. ; Miller, P. D. ; Cronin, R. E. / Effects of furosemide and acetylcholine in norepinephrine induced acute renal failure. American Journal of Physiology - Renal Fluid and Electrolyte Physiology. Vol. 4 2. ed. 1978.
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abstract = "The influence of intrarenal acetylcholine (ACh) or intravenous furosemide (F) on the course of norepinephrine (NE)-induced acute renal failure (ARF) was investigated in the dog. All groups received a 40-min intrarenal infusion of NE (0.75 μg/kg per min). Group I received NE alone; group II received ACh (20 μg/min) intrarenally which was started 30 min before NE infusion and continued throughout the study; and group III received F (10 mg/kg i.v.) before NE infusion followed by a constant infusion of F (10 mg/kg per h) throughout the study. In group IV F was started immediately after completion of NE infusion. All groups were studied before, during, and 3 h after NE infusion. Urine losses were replaced with a 0.9{\%} sodium chloride solution. Before NE, the mean glomerular filtration rate (GFR) in the infused kidney of groups I-IV was 54.1 ± 6.5, 44.2 ± 1.3, 50.2 ± 5.3, and 57.6 ± 7.3 ml/min, respectively. During NE, GFR and renal blood flow (RBF) were undetectable in the infused kidneys of all four groups. Three hours after NE GFR was 1.3 ± 1.3 in group I and 5.9 ± 4.9 ml/min in group II. In contrast, GFR in groups III and IV was 28.4 ± 5.4 and 15.40 ± 2.4 ml/min, respectively (P < 0.01 compared to group I). Before the NE infusion RBF was comparably and significantly increased from control in groups II and III. However, osmolar clearance C(osM) was increased before NE most profoundly in group III (9.04 ± 1.25 ml/min, P < 0.01 compared to groups I and II). In group IV, C(osM) increased to 7.13 ± 1.37 ml/min (P < 0.01 compared to group I). We conclude that F exerts a significant protective effect in this ischemic model of ARF, which could not be mimicked by ACh despite comparable increases in RBF. The higher C(osM) with F may be an important intratubular factor in the protection.",
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N2 - The influence of intrarenal acetylcholine (ACh) or intravenous furosemide (F) on the course of norepinephrine (NE)-induced acute renal failure (ARF) was investigated in the dog. All groups received a 40-min intrarenal infusion of NE (0.75 μg/kg per min). Group I received NE alone; group II received ACh (20 μg/min) intrarenally which was started 30 min before NE infusion and continued throughout the study; and group III received F (10 mg/kg i.v.) before NE infusion followed by a constant infusion of F (10 mg/kg per h) throughout the study. In group IV F was started immediately after completion of NE infusion. All groups were studied before, during, and 3 h after NE infusion. Urine losses were replaced with a 0.9% sodium chloride solution. Before NE, the mean glomerular filtration rate (GFR) in the infused kidney of groups I-IV was 54.1 ± 6.5, 44.2 ± 1.3, 50.2 ± 5.3, and 57.6 ± 7.3 ml/min, respectively. During NE, GFR and renal blood flow (RBF) were undetectable in the infused kidneys of all four groups. Three hours after NE GFR was 1.3 ± 1.3 in group I and 5.9 ± 4.9 ml/min in group II. In contrast, GFR in groups III and IV was 28.4 ± 5.4 and 15.40 ± 2.4 ml/min, respectively (P < 0.01 compared to group I). Before the NE infusion RBF was comparably and significantly increased from control in groups II and III. However, osmolar clearance C(osM) was increased before NE most profoundly in group III (9.04 ± 1.25 ml/min, P < 0.01 compared to groups I and II). In group IV, C(osM) increased to 7.13 ± 1.37 ml/min (P < 0.01 compared to group I). We conclude that F exerts a significant protective effect in this ischemic model of ARF, which could not be mimicked by ACh despite comparable increases in RBF. The higher C(osM) with F may be an important intratubular factor in the protection.

AB - The influence of intrarenal acetylcholine (ACh) or intravenous furosemide (F) on the course of norepinephrine (NE)-induced acute renal failure (ARF) was investigated in the dog. All groups received a 40-min intrarenal infusion of NE (0.75 μg/kg per min). Group I received NE alone; group II received ACh (20 μg/min) intrarenally which was started 30 min before NE infusion and continued throughout the study; and group III received F (10 mg/kg i.v.) before NE infusion followed by a constant infusion of F (10 mg/kg per h) throughout the study. In group IV F was started immediately after completion of NE infusion. All groups were studied before, during, and 3 h after NE infusion. Urine losses were replaced with a 0.9% sodium chloride solution. Before NE, the mean glomerular filtration rate (GFR) in the infused kidney of groups I-IV was 54.1 ± 6.5, 44.2 ± 1.3, 50.2 ± 5.3, and 57.6 ± 7.3 ml/min, respectively. During NE, GFR and renal blood flow (RBF) were undetectable in the infused kidneys of all four groups. Three hours after NE GFR was 1.3 ± 1.3 in group I and 5.9 ± 4.9 ml/min in group II. In contrast, GFR in groups III and IV was 28.4 ± 5.4 and 15.40 ± 2.4 ml/min, respectively (P < 0.01 compared to group I). Before the NE infusion RBF was comparably and significantly increased from control in groups II and III. However, osmolar clearance C(osM) was increased before NE most profoundly in group III (9.04 ± 1.25 ml/min, P < 0.01 compared to groups I and II). In group IV, C(osM) increased to 7.13 ± 1.37 ml/min (P < 0.01 compared to group I). We conclude that F exerts a significant protective effect in this ischemic model of ARF, which could not be mimicked by ACh despite comparable increases in RBF. The higher C(osM) with F may be an important intratubular factor in the protection.

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