Abstract
Objective: To investigate renal function and whether captopril prevents alterations in the handling of sodium and water in the ovarian hyperstimulation syndrome (OHSS) in the rabbit. Design: Experimental study Setting: Physiology laboratory. Animal(s): Six female New Zealand white rabbits were used as controls, and 13 were hyperstimulated with gonadotropins. Intervention(s): Saline or captopril. Main Outcome Measure(s): Renal excretory and hemodynamic variables. Result(s): The 3% extracellular volume expansion in OHSS animals induced a significant elevation in mean arterial pressure by 27%, although increments in natriuresis and diuresis were similar to those observed in controls. The OHSS group had impaired pressure-natriuresis sensitivity compared with controls (0.36 ± 0.07 μEq/min/g of Na excreted per mm Hg vs. 1.74 ± 0.45 μEq/min/g of Na excreted per mm Hg; P<.05. Captopril significantly reduced mean arterial pressure ( P<.05) and shifted the pressure-natriuresis response to the left by 0.85 ± 0.17 μEq/min/g of Na excreted per mm Hg ( P<.05). Conclusion(s): In OHSS in the rabbit model, pressure-natriuresis sensitivity is impaired. Angiotensin II may play a significant role in this phenomenon, since angiotensin-converting enzyme inhibition normalized the pressure-natriuresis relationship.
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