Effects of Angiotensin II and the AT&lt;sub&gt;1&lt;/sub&gt; Receptor Antagonist Losartan on the Renal Excretion of Urodilatin

Heringlake, Matthias; Bahlmann, Ludger; Klaus, Stephan; Wagner, Klaus; Schmucker, P.; Pagel, Horst

doi:10.1159/000054211

Cited by 3 publications

(4 citation statements)

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“…Of note, data from our group on the renal excretion of urodilatin -another member of the natriuretic peptide family produced in the kidney -have set up a potential role of AII in the regulation of the renal natriuretic peptide system as urodilatin excretion is decreased by AII in the isolated perfused rat kidney [2] . The present study was thus designed to determine, if the renal excretion of NTproBNP is also modulated by AII in humans.…”

Section: Discussionmentioning

confidence: 99%

“…Data from our group suggest a possible link between the renin-angiotensin system and the renal natriuretic peptide system [2] . The present study was thus designed to explore the effects of changes in angiotensin II (AII) plasma levels on sodium excretion, plasma and urinary levels of NTproBNP, and NTproANP plasma levels in healthy volunteers during intravenous sodium loading.…”

Section: Introductionmentioning

confidence: 86%

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The Effects of Angiotensin-Converting Enzyme Inhibition on the Urinary Excretion of NTproBNP in Male Volunteers

Heringlake¹,

Will²,

Klaus³

et al. 2006

Kidney Blood Press Res

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Aims: This study was designed to test if the renal excretion of the N-terminal prohormone of the B-type natriuretic peptide (NTproBNP) is modulated by angiotensin-converting enzyme inhibition (ACE-I). Methods: Following 7 days on a sodium-enriched diet and an induction period of 4 days with incremental dosages of enalapril (2.5, 5, 7.5, 10 mg) or placebo, 10 healthy subjects underwent crossover and double-blind treatment with 20 mg enalapril sodium or placebo at 8:00 h. After 4 h (at 12:00 h), 20 ml·kg^–1 NaCl 0.9% was infused over 60 min. Hemodynamics were determined and blood and urine were sampled at 8:00, 12:00, 13:00, 14:00, 16:00, and 18:00 h. Angiotensin II (AII), NTproANP, and NTproBNP were determined by radio- and electrochemiluminescence immunoassays. Results: In the whole group, ACE-I led to a lower arterial blood pressure during the fourth day of induction and during the time from 8:00 to 16:00 h, a decrease in AII levels from 8:00 to 14:00 h (p < 0.05), and to a higher cumulative urine output (p < 0.05) in comparison with control. Neither cumulative sodium nor urinary NTproBNP/creatinine excretion were significantly increased after ACE-I. However, a subgroup of 6 volunteers – showing an increase in sodium excretion after ACE-I – also demonstrated lower AII levels at 13:00 h, a higher cumulative urine flow, and a higher urinary NTproBNP/creatinine excretion in comparison with control (all: p < 0.05). Conclusions: This suggests that the renal excretion of NTproBNP is modified by enalapril. However, it remains to be determined if this is a direct effect of ACE-I, the decrease in arterial blood pressure, or other potentially confounding variables like bradykinin or endopeptidase activity.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 86%

The Effects of Angiotensin-Converting Enzyme Inhibition on the Urinary Excretion of NTproBNP in Male Volunteers

Heringlake¹,

Will²,

Klaus³

et al. 2006

Kidney Blood Press Res

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“…In brief, kidneys were perfused at constant pressure (100 mm Hg) in a recirculation system for 3 h. The perfusion medium was a substrate-and amino-acid-enriched Krebs-Henseleit buffer (pH 7.4) and was composed as already described [30] except that gentamicin sulfate was omitted. The medium was supplemented with predialyzed (3 !…”

Section: Kidney Perfusionmentioning

confidence: 99%

“…Drug concentrations and animal numbers were chosen according to our own data from pre-experiments [also reviewed in 22] and already published studies [28,31] . Stability of the isolated-perfused kidney is given for at least 3 h [30] . During this observation period an excellent stability of the whole experimental system, verified by small standard errors, was seen.…”

Section: Experimental Designmentioning

confidence: 99%

Urodilatin and Pentoxifylline Prevent the Early Onset of <i>Escherichia coli</i>-Induced Acute Renal Failure in a Model of Isolated Perfused Rat Kidney

Groesdonk

Bauer²,

Kreft³

et al. 2009

Kidney Blood Press Res

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Background/Aims: Raised cytokine levels and a hypoperfusion-associated decrease in glomerular filtration rate (GFR) are hallmarks of the genesis of septic acute renal failure (ARF). Therefore, anti-inflammatory as well as renal vasodilating therapeutic strategies may afford renal protection during septic ARF. The present study was designed to determine the effects of administration of urodilatin, pentoxifylline and theophylline to improve renal function in an ex-vivo model of ‘septic renal injury’. Methods: Eight series of experiments were performed: no intervention, perfusion with a suspension containing Escherichia coli bacteria (strain 536/21); E. coli + 10 μg/l urodilatin, E. coli + 20 μg/l urodilatin, E. coli + 100 μM theophylline, E. coli + 100 μM pentoxifylline and E. coli + URO 20 μg/l given 90 min after start of perfusion. Renal vascular and glomerular functional parameters as well as TNF-α release were analyzed up to 180 min. Results: Perfusion with E. coli caused an acute deterioration of renal vascular and glomerular function. URO 20 μg/l and PTX decreased renal vascular resistance (RVR) from 83.7 ± 18.4 to 9.2 ± 1.1 and 8.6 ± 2.2 mm Hg/ml/min/g kidney and increased renal perfusion flow rate (PFR) from 8.2 ± 1.5 to 14.6 ± 0.8 and 14.1 ± 2.2 ml/min/g kidney. As a result, GFR improved from 102.1 ± 15.6 to 442 ± 48.3 and 525.8 ± 57 μl/min/g kidney during treatment with URO 20 μg/l and PTX, respectively. Renal TNF-α release was significantly reduced by URO 20 μg/l (from 178 ± 23 to 45.2 ± 2 and 47 ± 3 pg/ml) in the E. coli + URO 20 μg/l and by PTX in the E. coli + PTX group if added to the perfusion medium upon start of perfusion. Interestingly, URO 20 μg/l also decreased RVR significantly from 62.2 ± 6.1 to 35.9 ± 6.0 mm Hg/ml/min/g kidney, improved PFR from 5.4 ± 1.0 to 8.7 ± 1.0 ml/min/g kidney, increased GFR from 160 ± 43.3 to 280.7 ± 27.9 μl/min/g kidney, and decreased TNF-α release to 122 ± 18 pg/ml if applied 90 min after induction of septic ARF. In contrast, URO 10 μg/l did not significantly increase urine flow and did not appear to significantly improve renal perfusion. Theophylline showed no beneficial effects at all. Conclusion: This suggests that urodilatin and pentoxifylline might be useful to protect renal function if given before a septic renal insult. Additionally, treatment with urodilatin is capable of restoring renal function in early Gram-negative sepsis-induced ARF even if given after the septic insult.

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Natriuretic Peptides

Campese¹

2005

Hypertension

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Effects of Angiotensin II and the AT<sub>1</sub> Receptor Antagonist Losartan on the Renal Excretion of Urodilatin

Cited by 3 publications

References 4 publications

The Effects of Angiotensin-Converting Enzyme Inhibition on the Urinary Excretion of NTproBNP in Male Volunteers

The Effects of Angiotensin-Converting Enzyme Inhibition on the Urinary Excretion of NTproBNP in Male Volunteers

Urodilatin and Pentoxifylline Prevent the Early Onset of <i>Escherichia coli</i>-Induced Acute Renal Failure in a Model of Isolated Perfused Rat Kidney

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