1. We tested the effects of blockade of nitric oxide synthesis on renal function under conditions of controlled renal artery pressure. Our hypothesis was that endogenous nitric oxide plays a role in the natriuresis that accompanies increased renal perfusion pressure. We used a novel technique which employed an extracorporeal circuit to produce step changes over a wide range of renal artery pressures in pentobarbitone‐anaesthetized rabbits. 2. Rabbits were treated with either NG‐itro‐l‐arginine (NOLA, 20 mg/kg, i.v.; n = 8) or its vehicle (n= 8). Renal artery pressure was set (by adjusting the extracorporeal circuit) at 65, 80, 95, 110 and then 130mmHg respectively, at the beginning of each of five 30 min experimental periods. 3. NOLA treatment caused profound renal vasoconstriction that was largely independent of the level of renal artery pressure, renal blood flow being 35–43% lower in NOLA‐treated than in vehicle‐treated rabbits across the range of renal artery pressures tested (P= 0.002). NOLA treatment increased filtration fraction (P = 0.02), and tended to reduce glomerular filtration rate (P= 0.09). 4. NOLA‐treatment affected sodium excretion in a manner dependent on the level of renal artery pressure, with the slope of the relationship between sodium excretion and renal artery pressure being lower in NOLA‐treated than in vehicle‐treated rabbits (P= 0.006). 5. These data provide direct evidence that in anaesthetized rabbits endogenous nitric oxide (i) tonically dilates the renal vasculature across a wide range of renal perfusion pressures, and (ii) enhances sodium excretion to a progressively greater degree as renal artery pressure is increased. It may therefore play a role in pressure‐induced natriuresis.
|Number of pages||8|
|Journal||Clinical and Experimental Pharmacology and Physiology|
|Publication status||Published - 1995|
- glomerular filtration
- nitric oxide, pressure natriuresis, renal blood flow, sodium homeostasis.