Increased tubuloglomerular feed-back mediated suppression of glomerular filtration during acute volume expansion in rats.

摘要: 1. Volume expansion is currently believed to change the intrinsic properties of juxtaglomerular apparatus such that sensitivity tubuloglomerular feedback (TGF) mechanism reduced, thus allowing glomerular filtration rate, and hence salt water excretion, rise. Recent studies conflict with this view indeed older literature reveals rise in rate (GFR) under these conditions far more modest than would be expected if TGF control were eliminated. 2. To investigate problem, was examined by measuring single-nephron (SNGFR) during loop Henle perfusion at varying rates rats conditions, after acute, moderate (4% body weight), iso-oncotic volume treated antibodies atrial natriuretic peptide (ANP) prior acute expansion. 3. With interrupted filtrate collection from proximal tubule, SNGFR expanded massively increased compared controls, although measured distal intact, only modestly increased, as whole-kidney rate. Loop increasing up 30 nl min-1 progressively decreased range over which exerted extended 60-80 min-1. For changes flow around spontaneous operating point, mechanism, defined delta SNGFR/delta flow, similar both groups. Treatment ANP substantially blunted renal excretion increase seen absence perfusion. 4. These results are not consistent a diminution function expansion, rather an enhancement. The latter best accounted for vasodilation preglomerular resistance vessels on result predicted calculations model based serial arrangement TGF-controlled vascular elements established pharmacological actions ANP.