Tubuloglomerular feedback during XXXX .

@entity8 @entity13645 @entity4247
Interstitial hydrostatic and oncotic pressures are believed to influence the sensitivity of the tubuloglomerular feedback (TGF) control. To further investigate this hypothesis, three groups of experiments with @entity8 ( @entity4247 ) were conducted. We investigated 1) the stop-flow pressure ( @entity13645 ) feedback response; 2) urine flow rate, glomerular filtration rate (GFR), subcapsular interstitial hydrostatic pressure (Psc), and interstitial oncotic pressure (pi int); and 3) the proximal-distal single nephron glomerular filtration rate (SNGFR). The results showed that the @entity13645 feedback response was unaffected by @entity4247 elevation. Psc increased from 0.5 to 3.5 mmHg and pi int increased from 2.1 to 5.8 mmHg; thus, no change in net interstitial pressure (Psc - pi int) was found during elevated @entity4247 . There was a significant proximal-distal SNGFR difference during both control and elevated @entity4247 (8.0 and 6.3 nl/min, respectively). A 20% reduction in total GFR and SNGFR was observed at increased @entity4247 . In separate experiments using the same protocol, a 5% body wt/h volume expansion with saline was induced before @entity4247 was elevated. During volume expansion, TGF sensitivity declined and net interstitial pressure increased, both of which were normalized by increasing @entity4247 . The results show that the TGF sensitivity is normal during elevated @entity4247 to 20 mmHg and that the increase in Psc during this condition is counter-balanced by an increase in pi int. In addition, the decrease in GFR and SNGFR during increased @entity4247 cannot be explained by a change in TGF activity. However, these findings indicate that both interstitial hydrostatic and oncotic pressures may influence the resetting of the TGF sensitivity.
