Key result
Coadministration of tolvaptan and BNP in experimental heart failure significantly increased urine flow (+2.4 mL/min) compared to tolvaptan alone (+0.4 mL/min) or BNP alone (+0.8 mL/min) (P<0.05).
Why the study?
Does the combination of tolvaptan and BNP improve renal excretory function without adversely affecting hemodynamics or activating aldosterone in experimental congestive heart failure?
Does the combination of tolvaptan and BNP improve renal excretory function without adversely affecting hemodynamics or activating aldosterone in experimental congestive heart failure?
Absolute Event Rate: 2.4% vs 0.4%
p-value: p=<0.05
Coadministration of tolvaptan and BNP in experimental heart failure provides potent diuresis and natriuresis without adverse hemodynamic effects or aldosterone activation.
Hypothesis-generating for combined diuretic use in experimental HF; leaves open human translation and safety.
BACKGROUND: Hemodynamic and neurohumoral function can affect the efficacy of diuretic therapy in congestive heart failure. Arginine vasopressin increases water reabsorption through the V(2) receptor in the collecting duct, whereas B-type natriuretic peptide (BNP) decreases sodium reabsorption in the collecting duct. We hypothesized that combining BNP to the V(2)-receptor antagonist tolvaptan (TLV) would enhance renal excretory function by augmenting sodium excretion together with aquaresis without adversely affecting renal hemodynamics in experimental congestive heart failure. METHODS AND RESULTS: Congestive heart failure was induced in 3 groups (n=6 per group) of dogs by tachypacing. A acute experiment was done after 10 days. After baseline measurements, study groups received a 0.1 mg/kg IV bolus of TLV alone (TLV), TLV in combination with BNP (TLV+BNP; 50 ng/[kg . min]), or BNP alone (BNP). Mean arterial pressure increased with TLV, remained unchanged with TLV+BNP, and decreased with BNP (+5+/-1mm Hg versus -1+/-1 mm Hg versus -15+/-1 mm Hg; P<0.05). Renal blood flow and glomerular filtration rate were preserved with all regimens. Urine flow increased in all 3 groups but significantly more so with TLV+BNP (TLV: +0.4+/-0.1 mL/min versus TLV+BNP: +2.4+/-0.5 mL/min versus BNP: +0.8+/-0.3 mL/min; P<0.05). Only TLV+BNP and BNP were natriuretic (P<0.05), whereas only TLV and TLV+BNP increased electrolyte-free water excretion (P<0.05). Compared with TLV alone, TLV+BNP prevented an increase in aldosterone (P<0.05). CONCLUSIONS: Coadministration of TLV and BNP in experimental HF resulted in a beneficial profile of renal, neurohumoral, and hemodynamic actions, specifically potent diuresis with natriuresis, neutral effect on mean arterial pressure, and lack of aldosterone activation.
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Costello‐Boerrigter et al. (2010) studied Experimental congestive heart failure (n=18). Tolvaptan in combination with BNP vs. Tolvaptan alone or BNP alone was evaluated on Urine flow (p=<0.05). Coadministration of tolvaptan and BNP in experimental heart failure significantly increased urine flow (+2.4 mL/min) compared to tolvaptan alone (+0.4 mL/min) or BNP alone (+0.8 mL/min) (P<0.05).
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