Cardiopulmonary baroreflex function in nephrotic rats.

Efferent renal sympathetic nerve activity is increased in experimental nephrotic syndrome and exhibits attenuated cardiopulmonary baroreflex inhibition during volume expansion in anesthetized rats. Additional studies were performed in conscious rats to avoid the potentially confounding influences of anesthesia; these studies used another more specific standardized stimulus for cardiopulmonary baroreflex activation. Sprague Dawley rats were studied 3 to 4 wk after adriamycin injection (3.5 mg/kg iv); all rats developed proteinuria. In sinoaortic denervated rats (anesthetized), graded frequency stimulation of the central end of the cut right vagus nerve produced frequency-dependent decreases in mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity. The decreases in mean arterial pressure and heart rate were similar in control and nephrotic rats, but efferent renal sympathetic nerve activity decreased significantly less in nephrotic than control rats over the entire frequency range (P < 0.02). In sinoaortic denervated rats (conscious), 10% body weight isotonic saline volume expansion decreased mean arterial pressure, heart rate, and efferent renal sympathetic nerve activity. The decreases in mean arterial pressure and heart rate were similar in control and nephrotic rats, but efferent renal sympathetic nerve activity decreased significantly less in nephrotic than control rats over the entire period of volume expansion (P < 0.04). In nephrotic syndrome, the cardiopulmonary baroreflex inhibition of efferent renal sympathetic nerve activity is decreased; the defect lies in the central portion of the reflex. This may contribute to the observed increase in efferent renal sympathetic nerve activity in nephrotic syndrome.