Key result
Acute hypervolemia potentiates renal responses but suppresses hypotensive effects of IV anaritide in monkeys.
Why the study?
The renal and hemodynamic effects of intravenous anaritide in conscious rhesus monkeys with and without acute extracellular hypervolemia were analyzed and compared to understand volume status influence.
Does intravenous anaritide affect renal and hemodynamic responses differently in conscious rhesus monkeys with and without acute extracellular hypervolemia?
Does intravenous anaritide affect renal and hemodynamic responses differently in conscious rhesus monkeys with and without acute extracellular hypervolemia?
Acute extracellular hypervolemia enhances the renal effects but blunts the hypotensive effects of anaritide in a primate model.
Hypervolemia may differentially modulate anaritide effects in primates; leaves open translation to human cardiorenal management.
The renal and hemodynamic responses to intravenous anaritide, a human atrial natriuretic factor [102-126] at 0.3 to 20 micrograms/kg in conscious rhesus monkeys with and without acute extracellular hypervolemia were analyzed and compared. Acute isotonic saline loading (intravenous bolus at 10 mL/kg plus continuous infusion at 0.25 mL/kg/min 30 min prior to and maintained throughout experiment) significantly augmented urine output (UV) and urinary Na+ excretion rate (UNaV) by 31% and 91%, respectively. Radial mean arterial pressure (MAP) and heart rate (HR) were not affected by volume expansion. Anaritide at doses higher than 0.3 micrograms/kg reduced MAP in a dose-dependent fashion in euvolemic monkeys. In contrast, reduction in MAP was observed only at the highest dose (20 micrograms/kg) of anaritide in hypervolemic monkeys. The hypotensive responses to anaritide at 20 micrograms/kg in euvolemic and hypervolemic animals were similar (-26 +/- 5 v -24 +/- 5 mm Hg, respective maximum changes in MAP). UV and UNaV were increased by anaritide at 3 to 20 micrograms/kg in both euvolemic and hypervolemic monkeys; however, the increases at each effective dose of anaritide were greater or tended to be greater in hypervolemic rhesus monkeys compared with euvolemic rhesus monkeys. Compared to vehicle responses, HR was not affected by anaritide in either group of animals. In conclusion, acute extracellular hypervolemia potentiates the renal but suppresses the hypotensive responses to anaritide in conscious rhesus monkeys.
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Lee et al. (1990) studied Acute extracellular hypervolemia. Anaritide (human atrial natriuretic factor [102-126]) vs. Vehicle / Euvolemic state was evaluated on Renal and hemodynamic responses (mean arterial pressure, heart rate, urine output, urinary Na+ excretion). In conscious rhesus monkeys, acute extracellular hypervolemia potentiated the renal responses but suppressed the hypotensive responses to intravenous anaritide.
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