Glomerular responses to platelet-activating factor in the rat: Role of thromboxane A2

K. F. Badr, D. K. DeBoer, K. Takahashi, R. C. Harris, A. Fogo, H. R. Jacobson

Research output: Contribution to journalArticlepeer-review

Abstract

In view of its role as a proinflammatory mediator in glomerular injury, we investigated the renal cortical microcirculatory responses to the intrarenal arterial administration of platelet-activating factor (PAF) in the anesthetized euvolemic Munich-Wistar rat. Close arterial administration of PAF led to dose-dependent reductions in renal plasma flow rate (RPF), glomerular filtration rate (GFR), and filtration fraction (FF), in the absence of hypotension or hemoconcentration. Single-nephron (SN) plasma flow rate (Q(A)), SNGFR and SNFF also fell [126 ± 7 to 101 ± 6 nl/min (P <0.005), 40.6 ± 2.1 to 21.5 ± 2.5 nl/min (P <0.005), and 0.33 ± 0.03 to 0.21 ± 0.03 (P <0.025)]. PAF increased pre- and postglomerular arteriolar resistances [2.32 ± 0.14 to 2.73 ± 0.19 (P <0.005) and 1.32 ± 0.13 to 1.45 ± 0.10 1010 dyn · s · cm-5 (P<0.05)]. PAF infusion also led to a dramatic reduction in the mean value for the glomerular capillary ultrafiltration coefficient, K(f) [0.058 ± 0.012 to 0.020 ± 0.003 nl · s-1 · mmHg (P <0.025)]. PAF-induced changes in renal hemodynamics were abolished in the presence of the cyclooxygenase inhibitors, indomethacin and ibuprofen. When administered concomitantly with a thromboxane A2 (TxA2) receptor antagonist, PAF led to significant increases in RPF and GFR. In isolated glomeruli, PAF stimulated the biosynthesis of TxB2 in a dose-dependent manner. Thus PAF depresses rat glomerular function by inducing contraction of arteriolar and mesangial smooth muscle. These effects are likely mediated via the secondary release of TxA2.

Original languageEnglish (US)
JournalAmerican Journal of Physiology - Renal Fluid and Electrolyte Physiology
Volume256
Issue number1
StatePublished - 1989
Externally publishedYes

ASJC Scopus subject areas

  • Physiology

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