title: Tubuloglomerular feedback in one-kidney, one-clip hypertensive rats.
abstract: Previous studies have shown that hydropenic one-kidney, one-clip (1-K, 1-C) hypertensive HT rats exhibit impaired autoregulation of glomerular filtration rate (GFR) in response to reduced arterial perfusion pressure. We investigated the possible role of altered tubuloglomerular feedback (TGF) activity in this phenomenon. Uninephrectomized Wistar rats were studied acutely 3 weeks after placing silver clips (0.2 mm) on the renal artery. Experiments were performed in 1-K,1-C HT rats and in uninephrectomized control animals. TGF activity was assessed as changes in proximal tubule stop-flow pressure (SFP) in response to orthograde microperfusion from 0 to 80 nl/min into late proximal tubule segments. Only the highest perfusion rates (approximately 40 nl/min) into late proximal tubule segments resulted in maximal decreases in SFP, indicating a marked rightward shift of overall TGF activity in 1-K,1-C HT rats. Similar responses were observed in the uninephrectomized animals. In contrast, changes of SFP were observed at lower perfusion rates in normal animals and maximal responses were observed at perfusion rates of approximately 20 nl/min. These observations are consistent with the possibility that altered TGF activity contributes to impaired autoregulation of GFR in 1-K,1-C HT rats in response to reduced renal perfusion pressure. In response to treatment with i.v. captopril, the 1-K,1-C HT rats exhibited marked decreases in systemic arterial pressure associated with decreases in SFP and virtually complete inhibition of TGF activity. It is attractive to hypothesize that these alterations in TGF characteristics in the 1-K,1-C HT rats play a significant pathophysiologic role in the acute renal dysfunction observed in response to acute decreases of blood pressure during conditions of augmented angiotensin activity. Additional future studies will allow us to address the precise role for intrarenal angiotensin in these phenomena.
authors.affiliation: Division of Nephrology, Medical of South Carolina, Charleston.
authors.forename: D W
authors.initials: DW
authors.lastname: Ploth
authors.forename: H S
authors.initials: HS
authors.lastname: Mackenzie
mesh_terms: D000804:Angiotensin II / Q000502:physiology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects / Q000502:physiology; D002216:Captopril / Q000494:pharmacology; D005246:Feedback; D006978:Hypertension, Renovascular / Q000503:physiopathology*; D007678:Kidney Glomerulus / Q000503:physiopathology*; D007684:Kidney Tubules / Q000503:physiopathology*; D051381:Rats; D011919:Rats, Inbred Strains
chemical_list: D000804:Angiotensin II; D002216:Captopril