The authors used techniques to examine the intrarenal response to an acute elevation of the renal perfusion pressure. In one series of studies (epinephrine, group I) the renal perfusion pressure was acutely increased by intravenous epinephrine infusion; in another series, by bilateral carotid occlusion and vagotomy. A third series of studies (epinephrine, group II) was performed identically to the epinephrine, group I, studies except that the renal perfusion pressure was held constant during the epinephrine infusion by suprarenal aortic constriction. After epinephrine infusion (group I) and following bilateral carotid occlusion and vagotomy the renal perfusion pressure increased, from 119 ± 1.0 (SEM) to 166 ± 1.85 mm Hg and from 122 ± 5.9 to 168 ± 3.1 mm Hg, respectively. Fractional sodium excretion rose from 2.31 ± 0.34% to 5.09 ± 0.58% (P<0.001) after epinephrine and from 1.80 ± 0.71% to 6.40 ± 1.0% (P<0.001) following carotid occlusion and vagotomy. In neither study, however, did the authors find that the increase in renal perfusion pressure changed the glomerular filtration rate (GFR) (both kidneys) or fractional sodium delivery from the superficial cortical late distal tubule. Furthermore, they found that epinephrine infusion at a constant renal perfusion pressure (epinephrine, group II) did not affect fractional sodium excretion, although a small, but significant decrease in the GFR and sodium delivery from the superficial late distal tubule occurred. These data suggest that the natriuresis which follows an acute elevation of the renal perfusion pressure cannot be attributed to enhanced sodium delivery from superficial nephrons but must result from (1) inhibition of sodium reabsorption in inner cortical nephrons or (2) an effect on sodium transport in the collecting system.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine