Atrial natriuretic factor inhibits maximal tubuloglomerular feedback response.
The effect of atrial natriuretic factor (ANF) on maximal tubuloglomerular feedback was assessed in 16 Munich-Wistar rats. When the loop of Henle was not perfused, ANF increased single nephron glomerular filtration rate (SNGFR) and stop-flow pressure (SFP) from 32 +/- 2 nl/min and 32 +/- 2 mmHg in the control period to 37 +/- 2 nl/min (P less than 0.05) and 40 +/- 2 mmHg (P less than 0.025) after ANF administration, respectively. Because ANF caused SFP to rise but did not significantly alter plasma protein concentration, the estimated glomerular capillary hydraulic pressure increased. Maximal tubuloglomerular feedback response (examined by increasing orthograde microperfusion of the loop from 0 to 50 nl/min) was significantly inhibited by ANF; changes in SNGFR and SFP during the control state, -9 +/- 2 nl/min and -9 +/- 1 mmHg, were reduced to -4 +/- 2 nl/min (P less than 0.05) and -5 +/- 1 mmHg (P less than 0.05), respectively, after ANF administration. In conclusion, the increase in SNGFR caused by ANF is associated with an increase in glomerular capillary hydraulic pressure and with a blunted maximal tubuloglomerular feedback response.
D000818:Animals; D009320:Atrial Natriuretic Factor / Q000494:pharmacology*; D001696:Biomechanical Phenomena; D005246:Feedback; D006439:Hemodynamics / Q000187:drug effects; D007678:Kidney Glomerulus / Q000098:blood supply / Q000187:drug effects* / Q000502:physiology; D007684:Kidney Tubules / Q000187:drug effects* / Q000502:physiology; D008297:Male; D051381:Rats; D011919:Rats, Inbred Strains
D009320:Atrial Natriuretic Factor