AJP - Renal Physiology, Vol 256, Issue 1 152-F157, Copyright © 1989 by American Physiological Society

ARTICLES

Intrarenal vasoconstriction during hyperchloremia: role of thromboxane

E. M. Bullivant, C. S. Wilcox and W. J. Welch
Department of Medicine, University of Florida School of Medicine, Gainesville.

The role of thromboxane (Tx) in chloride-induced renal vasoconstriction was studied in Munich-Wistar rats. Hyperchloremia (induced by changing an intra-aortic, super-renal infusion of 1.2 M Na acetate to 1.2 M NaCl) reduced the glomerular filtration rate (GFR) by 31 +/- 3% (P less than 0.001; n = 27), and the clearance of p-aminohippurate (CPAH) by 36 +/- 4% (P less than 0.01). The Tx synthetase antagonists (25 mg/kg) UK-38,485 or OKY-046 prevented these changes. Pretreatment with indomethacin (5 mg/kg) also prevented Cl-induced changes in GFR and CPAH and blunted (P less than 0.05) the Cl-induced increase in renal vascular resistance (RVR, vehicle +55 +/- 11%, n = 8, indomethacin +27 +/- 7%, n = 6). Hyperchloremia reduced the hydraulic pressures (mmHg) in the outer cortical efferent arteriolar star vessels (PEA, 23.9 +/- 1.6 vs. 17.9 +/- 0.9; P less than 0.01) and proximal tubules (PT, 21.1 +/- 1.5 vs. 15.8 +/- 1.4; P less than 0.01) but not in the glomerular capillaries (PGC, 47.0 +/- 2.5 vs. 49.5 +/- 2.2; NS). Therefore the hydraulic pressure drop across the glomerular capillaries (PGC - PT) increased (24.9 +/- 2.8 vs. 34.6 +/- 2.9; P less than 0.02). UK-38,485 prevented significant Cl-induced changes in these pressures. The calculated resistances of the afferent and efferent arterioles both increased during hyperchloremia (+56 +/- 19%; P less than 0.05 and +195 +/- 66%; P less than 0.01, respectively) but were blunted after UK-38,485 (+23 +/- 8 and +21 +/- 10%, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

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