Urodilatin is involved in sodium homeostasis and exerts sodium-state-dependent natriuretic and diuretic effects

Meyer, M Cobas; Richter, Rudolf; Brunkhorst, Reinhard; Wrenger, Eike; Schulz‐Knappe, Peter; Kist, Alwyn; Mentz, P; Brabant, E. G.; Koch, Karl-Martin; Rechkemmer, Gerhard; Forssmann, W. G.

doi:10.1152/ajprenal.1996.271.3.f489

Cited by 19 publications

(27 citation statements)

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“…Urodilatin is exclusively found in urine and in the kidney suggesting that it participates in the intrarenal regulation of sodium homoeostasis in a paracrine manner, but its physiological function is still incompletely understood [10,11]. Since urodilatin appears to contribute to the sodium excretion during hypervolaemic states [12], we hypothesized that the radiocontrast-induced diuresis may be associated with an increased urodilatin excretion. Therefore we measured the fractional excretion of sodium and urodilatin in the urine, as well as the plasma concentrations of atrial natriuretic peptide and creatinine in patients before and after coronary angiographic procedures to test the hypotheses that a) the diuresis following intravascular radiocontrast administration is a natriuresis which b) correlates with the urinary excretion of urodilatin.…”

Section: Introductionmentioning

confidence: 99%

Radiocontrast‐induced natriuresis associated with increased urinary urodilatin excretion

Haller

Meyer²,

Scheele

et al. 1998

Journal of Internal Medicine

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Abstract. Haller C, Meyer M, Scheele T, Koch A, Forssmann W-G and Kübler W (University of Heidelberg; and Lower Saxony Institute for Peptide Research, Hanover; Germany). Radiocontrastinduced natriuresis associated with increased urinary urodilatin excretion (original article). J Intern Med 1998; 243: 155-62.Objective. Intravascular radiocontrast agents induce a pronounced diuresis. The aim of the present study was to investigate the (patho-)physiological mechanisms of the radiocontrast-induced diuresis. Design. The fractional excretion of sodium, the urinary excretion of the renal natriuretic peptide urodilatin and the plasma concentration of atrial natriuretic peptide were measured in 42 unselected patients immediately before and after intravascular radiocontrast administration during coronary angiography. Setting. Cardiac catheterization laboratory of a university hospital. Results. After angiography both the plasma concentration of atrial natriuretic peptide (median post-pre difference: 3.9 pmol L Ϫ1 , quartiles Ϫ1.2; 7.0) and the urinary excretion of urodilatin (median post-pre difference: 67.0 nmol urodilatin/mol creatinine, quartiles 39.7; 152.1) were increased. The urinary urodilatin excretion was correlated with an increase in the fractional excretion of sodium (median post-pre difference: 1.7%, quartiles 0.6; 3.1). There was no correlation between the serum concentration of atrial natriuretic peptide and urinary sodium excretion. For the radiocontrast-induced increase in both urodilatin and sodium excretion there was no indication for differences between patients without (31) and with (11) intravenous saline infusion. Conclusion. The radiocontrast-induced diuresis is a natriuresis which is associated with an increased urinary excretion of urodilatin. The association between natriuresis and urinary urodilatin excretion irrespective of baseline volume status corroborates the hypothesis that urodilatin contributes to the sodium excretion after radiocontrast administration in a paracrine manner. This finding has pathophysiological and potentially therapeutic implications in radiocontrast-induced nephropathy.

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Section: Introductionmentioning

confidence: 99%

Radiocontrast‐induced natriuresis associated with increased urinary urodilatin excretion

Haller

Meyer²,

Scheele

et al. 1998

Journal of Internal Medicine

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“…And indeed, baseline urinary NTproBNP was higher in the present study than in the previous one [1] , while volume loading did not induce a further increase in this parameter. In contrast to this, Meyer et al [14] have shown a more pronounced increase in the excretion of the renal natriuretic peptide urodilatin following intravenous sodium loading during a sodium-enriched diet in comparison with a low-sodium state. This discrepancy cannot be solved by the present data.…”

Section: Discussionmentioning

confidence: 87%

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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“…So far, most studies dealing with the mechanisms regulating excretion and production of the natriuretic peptide urodilatin have focussed on the effects of different sodium loads [1], variations in central thoracic blood volume [4] and renal perfusion pressure [2] on U URO V. However, it is unclear which, if any, humoral factors mediate these effects at the level of the kidney. Since the renin-angiotensin system is also involved in the regulation of sodium and water homeostasis and renal perfusion pressure [5], this hormonal system likely interferes with U URO V.…”

Section: Discussionmentioning

confidence: 99%

“…The mechanisms regulating the production and excretion of the kidney-derived peptide urodilatin (ANP-95-126), which is presumed to act as a paracrine hormone in the regulation of sodium and water homeostasis, remain to be illucidated [1].…”

Section: Introductionmentioning

confidence: 99%

“…The urinary excretion of urodilatin (U URO V) has been shown to be influenced by variations in sodium load [1] Heringlake/Bahlmann/Klaus/Wagner/ Schmucker/Pagel and renal perfusion pressure [2], suggesting a possible interaction of the urodilatin system with the renin-angiotensin system. Hence we investigated the effects of angiotensin II (AII) and the AT 1 receptor antagonist losartan (LS) on U URO V and renal function in an isolated perfused rat kidney model.…”

Section: Introductionmentioning

confidence: 99%

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

Heringlake

Bahlmann²,

Klaus³

et al. 2001

Kidney Blood Press Res

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Background: The precise mechanisms regulating the natriuretic peptide urodilatin (ANP-95-126) remain to be defined. Renal excretion of urodilatin (U_UROV) has been shown to be modified by variations in plasma sodium and renal perfusion pressure. This suggests a relationship between urodilatin and the renin-angiotensin system. Methods: We investigated the effects of angiotensin II (AII, 0.1 nmol/l) and the AT₁ receptor antagonist losartan (LS, 1 µmol/l) on U_UROV and renal function in isolated rat kidneys perfused for 180 min in a closed circuit system. A further series employing a vasoconstricting concentration of endothelin-1 (ET-1, 0.01 nmol/l) was performed to explore the effects of vasoconstriction and glomerular filtration rate (GFR) on U_UROV. Results: Urine flow (UV) and urinary sodium excretion (U_NaV) decreased and renal vascular resistance (RVR) increased after treatment with AII (n = 5) in comparison with a control group (n = 6; p < 0.05). Treatment with LS (n = 5) and AII+LS (n = 5) had no significant effect on these parameters. GFR decreased after AII (p < 0.05) and was not significantly altered by other interventions. U_UROV decreased after AII (p < 0.05) and was comparable to the control group after LS and AII+LS. ET-1 (n = 5) induced a significant increase in RVR and decreased UV and U_NaV (p < 0.05). Point-to-point analysis revealed that the ET-1-induced vasoconstriction and the subsequent decrease in GFR had no effect on U_UROV. Conclusions: This suggests that vasoconstrictory concentrations of AII decrease U_UROV in the isolated perfused rat kidney. The lack of effect of ET-1 on U_UROV suggests that the AII-induced alterations in urodilatin excretion cannot be explained by vasoconstriction per se.

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Urodilatin is involved in sodium homeostasis and exerts sodium-state-dependent natriuretic and diuretic effects

Cited by 19 publications

References 0 publications

Radiocontrast‐induced natriuresis associated with increased urinary urodilatin excretion

Radiocontrast‐induced natriuresis associated with increased urinary urodilatin excretion

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

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

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