Feedback mediation of SNGFR autoregulation in hydropenic and DOCA- and salt-loaded rats.
Tubuloglomerular feedback (TGF) mediation of autoregulation was investigated by measuring the response of single nephron glomerular filtration rate (SNGFR) to changes in arterial pressure (AP) following acute or chronic TGF inhibition. In hydropenic rats with intact TGF, distal SNGFR was 25.0 +/- 1.2 (SE) and 23.9 +/- 1.4 nl/min at AP of 111 and 135 mmHg, respectively. In the same 20 nephrons during proximal tubular microinfusion of furosemide, distal SNGFR was 23.6 +/- 1.4 (n = 16) and 29.7 +/- 1.4 nl/min (n = 20) (P less than 0.001, n = 16) at 112 and 133 mmHg. When determined proximally, SNGFR was 25.6 +/- 1.0 and 29.5 +/- 0.9 nl/min (P less than 0.001, n = 31) at 112 and 157 mmHg; kidney GFR increased similarly. These data and the predictions of a GFR model were then used to estimate autoregulatory efficiency. This analysis indicated that partial autoregulation occurred during TGF inhibition. Therefore, TGF is an essential, but probably not the only, mechanism mediating SNGFR autoregulation.
D000042:Absorption; D000818:Animals; D002339:Carotid Arteries; D002712:Chlorides; D003681:Dehydration; D003900:Desoxycorticosterone / Q000494:pharmacology*; D005246:Feedback; D005665:Furosemide; D005919:Glomerular Filtration Rate; D006706:Homeostasis / Q000187:drug effects; D008297:Male; D009399:Nephrons / Q000502:physiology*; D051381:Rats; D012965:Sodium Chloride / Q000494:pharmacology*
D002712:Chlorides; D003900:Desoxycorticosterone; D012965:Sodium Chloride; D005665:Furosemide