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ANG II dependence of tubuloglomerular feedback responsiveness in hypertensive ren-2 transgenic rats.

TitleANG II dependence of tubuloglomerular feedback responsiveness in hypertensive ren-2 transgenic rats.
Publication TypeJournal Article
Year of Publication1995
AuthorsMitchell KD, Mullins JJ
JournalAm J Physiol
Volume268
Issue5 Pt 2
PaginationF821-8
Date Published1995 May
ISSN0002-9513
KeywordsAngiotensin II, Angiotensin Receptor Antagonists, Animals, Animals, Genetically Modified, Blood Pressure, Feedback, Glomerular Filtration Rate, Hemodynamics, Hydrostatic Pressure, Hypertension, Imidazoles, Kidney Glomerulus, Kidney Tubules, Male, Rats, Renal Circulation, Tetrazoles
Abstract

The present study was performed to determine the angiotensin II (ANG II) dependence of stop-flow pressure (SFP) tubuloglomerular feedback responses in hypertensive transgenic rats [strain name: TGR(mRen2)27] harboring the mouse ren-2 renin gene. SFP feedback responses to increases in late proximal perfusion rate were assessed in pentobarbital-anesthetized male ren-2 transgenic rats during control conditions and after administration of the AT1 receptor antagonist, L-158,809 (1 mg/kg iv). During control conditions, increases in late proximal perfusion rate elicited flow-dependent decreases in SFP. The magnitude of the maximal SFP feedback response to a late proximal perfusion rate of 40 nl/min averaged 16.1 +/- 1.4 mmHg (n = 7), a value higher than that normally observed in normotensive rats. Administration of L-158,809 decreased mean arterial blood pressure (174 +/- 6 vs. 117 +/- mmHg, P < 0.01, n = 10) and attenuated the magnitude of the maximal SFP feedback response by 84 +/- 4% (16.1 +/- 1.4 vs. 2.6 +/- 0.5 mmHg, P < 0.01, n = 7). In contrast, mechanical reduction of renal arterial pressure from 179 +/- 5 to 113 +/- 1 mmHg (P < 0.01, n = 7) attenuated the magnitude of the maximal SFP feedback response by only 43 +/- 5% (14.4 +/- 1.9 vs. 7.9 +/- 0.7 mmHg, P < 0.01, n = 7), indicating that approximately one-half of the attenuation of SFP feed-back responses elicited by AT1 receptor blockade was due to removal of the stimulatory effect of ANG II on the sensitivity of the tubuloglomerular feedback mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Alternate JournalAm. J. Physiol.
PubMed ID7771510