scholarly journals Vasopressin-2-receptor antagonism augments water excretion without changes in renal hemodynamics or sodium and potassium excretion in human heart failure

2006 ◽  
Vol 290 (2) ◽  
pp. F273-F278 ◽  
Author(s):  
Lisa C. Costello-Boerrigter ◽  
William B. Smith ◽  
Guido Boerrigter ◽  
John Ouyang ◽  
Christopher A. Zimmer ◽  
...  

Diuretics are frequently required to treat fluid retention in patients with congestive heart failure (CHF). Unfortunately, they can lead to a decline in renal function, electrolyte depletion, and neurohumoral activation. Arginine vasopressin (AVP) promotes renal water reabsorption via the V2 receptor, and its levels are increased in CHF. This study was designed to assess the effects of a single oral dose of tolvaptan, a selective V2-receptor blocker, in the absence of other medications, on renal function in human CHF and to compare this to the effects of a single oral dose of furosemide. We hypothesized that V2-receptor antagonism would yield a diuresis comparable to furosemide but would not adversely affect renal hemodynamics, plasma electrolyte concentration, or neurohumoral activation in stable human CHF. Renal and neurohumoral effects of tolvaptan and furosemide were assessed in an open-label, randomized, placebo-controlled crossover study in 14 patients with NYHA II-III CHF. Patients received placebo or 30 mg of tolvaptan on day 1 and were crossed over to the other medication on day 3. On day 5, all subjects received 80 mg of furosemide. Tolvaptan and furosemide induced similar diuretic responses. Unlike tolvaptan, furosemide increased urinary sodium and potassium excretion and decreased renal blood flow. Tolvaptan, furosemide, and placebo did not differ with respect to mean arterial pressure, glomerular filtration rate, or serum sodium and potassium. We conclude that tolvaptan is an effective aquaretic with no adverse effects on renal hemodynamics or serum electrolytes in patients with mild to moderate heart failure.

1998 ◽  
Vol 76 (1) ◽  
pp. 63-67 ◽  
Author(s):  
María Reverte ◽  
Olga Flores ◽  
Belén Gallego ◽  
Antonio Lestón ◽  
José Miguel López-Novoa

We have studied during 30 days the effect of a low dose of NG-nitro-L-arginine methyl ester (1 mg ·kg-1 ·day-1 in drinking water) in the presence of D- or L-arginine (1 mg ·kg-1 ·day-1 in drinking water) in comparison with D- or L-arginine alone on blood pressure and renal function in conscious uninephrectomized female spontaneously hypertensive rats. At the end of the study, there was a significant increase in systolic blood pressure in the NG-nitro-L-arginine methyl ester + D-arginine group (307 ± 6 mmHg (1 mmHg = 133.3 Pa), n = 14, p << 0.05) in comparison with NG-nitro-L-arginine methyl ester + L-arginine (281 ± 6 mmHg, n = 14), L-arginine (262 ± 5 mmHg, n = 13), and D-arginine (258 ± 7 mmHg, n = 12) groups. There were no changes in diuresis, proteinuria, or sodium and potassium excretion between differently treated animals during this study. These results suggest that in uninephrectomized female spontaneously hypertensive rats, after 1 month blockade of NO synthesis with a low dose of NG-nitro-L-arginine methyl ester, vasculature is under tonic control by NO and it is not correlated with renal dysfunction.Key words: Key words: NG -nitro-L-arginine methyl ester (L-NAME), kidney, hypertension, spontaneously hypertensive rats, renaldysfunction, uninephrectomy.


2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
Vesna Ristovska

Abstract Background and Aims The advanced congestive heart failure (CHF), may provoke functional kidney disturbances with insufficient and resistant to conservative therapy water excretion. The treatment of the chronic renal failure (CRF) with active dialysis related to ultrafiltration (UF), may overcome the renal diuretics resistance with diuresis restoration and oedema elimination. The aim of the study was to define the indications for active, discontinued UF in setting of the CHF refractory to drugs, especially in the treatment of oedema. Method We investigated 12 patients, mean age 62,4+/-5,3 years, with incipient renal failure, but advanced congestive heart failure. Seven of them were males and 5 females. The indication for discontinued UF, was the severe expressed heart failure, reduced diuresis and initial renal insufficiency. In all investigated patients, before and after each UF procedure, the serum sodium and potassium, blood urea nitrogen (BUN), creatinin and osmolality were detected. The body weight, abdominal and crural parameters were noted before and after dialysis. Results The recovery was achieved in 10 patients with CHF, but 2 patients out of 12 have not demonstrated satisfactory response to UF. The biochemical features encountered to CHF patients suggest chronic hyponatriemia, hypokalemia and hypovolemia. Proteinuria range 1,2 to 3,6 g/l, was present in 6 patients. The clinical data were performed with oedema formation, reduced diuresis and dispnea. Mean UF rate achieved after several dialysis was 12,4+/- 7,6, lit. Conclusion Chronic heart failure in chronic renal patients, with severe oedemas is an indication for UF therapy, even if the values of BUN and creatinin are not increased. Reduction of the body weight and the extracellular volume, contribute for improved survival in these patients. However the risk of complications is high and not always with successful treatment.


2000 ◽  
Vol 49 (3) ◽  
pp. 215-222 ◽  
Author(s):  
D. Y. Mitchell ◽  
J. V. St. Peter ◽  
R.A. Eusebio ◽  
K. A. Pallone ◽  
S. C. Kelly ◽  
...  

Author(s):  
Daisuke Miyatake ◽  
Tomohisa Shibata ◽  
Mai Shibata ◽  
Yuichiro Kaneko ◽  
Kazuo Oda ◽  
...  

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Fernando L Martin ◽  
Brenda K Huntley ◽  
Gerald E Harders ◽  
Sharon M Sandberg ◽  
Horng H Chen ◽  
...  

Background : Studies in human myocardial infarction (MI) suggest that even in the absence of heart failure (HF) alterations in renal function may occur and contribute to poor outcomes. After MI a decline in renal function may be seen acutely by mechanisms which are unclear. The long term consequences of MI upon renal function and structure remain poorly defined. We hypothesized that even without pre-existing renal disease, renal functional and structural changes would be present following MI. Methods : Cardiorenal function and structure were assessed in Wistar rats, Sham (S; n=10) and MI groups (n=9) 3 weeks after MI. GFR was determined by inulin clearance. Blood was obtained for PRA and aldosterone. Hearts and kidneys were harvested for histological analysis. Cardiac function was assessed by echo. Genome-wide microarray analysis was performed on kidney cortex (KC) and medulla (KM) (Affymetrix GeneChip® Rat Genome 230 2.0). Results : EF decreased after MI (S:62.8±2.3, MI:42.8±6.5 %, p<0.01) and LVEDd increased (p<0.005) PRA and aldosterone activation were absent. Blood pressure (BP) was not different between groups. There was no HF as sodium and water excretion was maintained. GFR tended to decrease (S:2.9±0.3, MI:2.4±0.2 ml/min, NS). Picrosirius Red staining for collagen in the KC and KM after MI showed greater fibrosis especially in the RM (KC S:1.1±0.2, MI:3.5±0.6 %, p<0.001 and KM S:1±0.2, MI:18.8±6 %, p<0.005). Microarray analysis revealed that 303 genes significantly changed in KM and 407 genes in the KC after MI (1.5 fold, P<0.05). Gene dysregulation was related to cell proliferation, metabolic processes and cell communication (Z value>2). Conclusion : We conclude that experimental MI results in renal structural remodeling characterized by renal cortical and medullary fibrosis with a mild reduction in GFR and extensive modulation of molecular pathways related to renal growth and metabolism. This investigation provides evidence for a heart-kidney connection after MI by mechanisms which remain to be defined. We also conclude that therapies for MI targeting the heart also should be evaluated for properties of renoprotection.


Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Susanne Jung ◽  
Agnes Bosch ◽  
Julie Kolwelter ◽  
Kristina Striepe ◽  
Dennis Kannenkeril ◽  
...  

Introduction: Chronic heart failure (CHF) and impaired renal function are two co-existing medical conditions and known to be associated with adverse outcome. The cardiorenal interaction has not yet been analyzed thoroughly. The aim of this study was to assess renal and intraglomerular hemodynamics by constant infusion input clearance technique in subjects with CHF compared to healthy controls. Methods: This was a cross-sectional observational study including 85 subjects. The group of subjects with CHF consisted of 27 individuals with HFpEF and 27 individuals with HFrEF, who were compared to 31 controls. All subjects underwent renal clearance examination to determine measured -not estimated- glomerular filtration rate (GFR), renal blood and plasma flow (RBF, RPF) and to calculate renal hemodynamic parameters such as filtration fraction (FF), renal vascular resistance (RVR), intraglomerular pressure (P glom ) and resistances of the afferent (R A ) and efferent arterioles (R E ). Results: GFR was lower in subjects with CHF (88.6±13.1ml/min/1.73m 2 ) compared to controls (108.6±17. ml/min/1.73m 2 ) after adjustment for age and BP (p adj =0.037). There were no significant differences regarding RPF, RBF, FF, RVR, P glom , R A as well as R E after adjustment for age and BP. Similarly, there were no significant differences regarding renal hemodynamic parameters between HFpEF and HFrEF subjects. Bivariate correlation analysis in the group of subjects with CHF revealed an inverse association between NT-proBNP and RPF (R=-0.421, p=0.002), RBF (R=-0.414, p=0.002) and a positive association with FF (R=0.324, p=0.019), RVR (R=0.346, p=0.012) and R E (R=0.318, p=0.022). Conclusions: The findings of this study indicate that in CHF renal function is slightly reduced even though renal perfusion is preserved. With progressive severity of CHF as indicated by increasing NT-proBNP, renal vascular resistance in particular at the postglomerular side increases. Our data are in accordance with neuroendocrine activation in CHF since vasoconstriction at the postglomerular site points towards angiotensin II as mediator. The association between NT-proBNP and renal hemodynamics documents a close cardiorenal interaction in CHF.


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