We investigated the relation between renal perfusion pressure and the release of a renal vasodepressor substance in vivo to determine whether this substance was released at physiological pressures. We perfused the left kidneys of anesthetized rabbits using an extracorporeal circuit that allowed renal perfusion pressures to be set at 65 mm Hg (control) and increased to 95, 125, 155, or 185 mm Hg for 30-minute experimental periods. Systemic blood pressure did not change significantly when renal perfusion pressure was maintained at 65 mm Hg throughout. When renal perfusion pressure was increased to 95, 125, 155, or 185 mm Hg, systemic blood pressure fell significantly at rates of 0.17±0.04, 0.79±0.31, 0.60±0.11, and 2.18±0.79 mm Hg/min, respectively (P<.05). Restoration of renal perfusion pressure to 65 mm Hg abruptly reversed the falls in systemic blood pressure in each group. There was a natriuresis and diuresis that were both pressure related and progressive in the face of each constant level of increased renal perfusion pressure. In summary, there was a continuum of arterial vasodepressor responses across a renal perfusion pressure range from resting pressure to 185 mm Hg. We suggest that the threshold level for the release of significant amounts of a renal medullary depressor substance, probably medullipin, is just above normal arterial blood pressure and that the rate of release increases with increasing arterial pressure.
|Number of pages||7|
|Publication status||Published - May 1994|
- blood pressure
- kidney medulla
- renal circulation