Effect of premercurial resetting of intrarenal vascular resistance on HgCl2-induced acute renal failure.
The role of renal hemodynamics in the first hours of HgCl2-induced acute renal failure was examined by studying the influence of resetting the total renal vascular resistance (RT) within the limits of autoregulation before and after the mercury administration. Intravenous HgCl2 alone (3 mg/kg) caused an early fall of glomerular filtration rate (GFR) from 69 +/- 3 to 38 +/- 4 ml/min/100 gm kidney weight (KW) and of renal blood flow (RBF) from 535 +/- 42 to 276 +/- 27 ml/min/100 gm KW, 3 hours after HgCl2 (P less than 0.01). In a second series, the RT was decreased by clamping the aorta before and after HgCl2 so that the mean renal perfusion pressure (MRPP) was lowered to a mean of 87 +/- 5 mm Hg). This maneuver did not prevent the fall in GFR (from 81 +/- 5 to 36 +/- 6 ml/min/100 gm KW) or in RBF (from 510 +/- 79 to 197 +/- 20 ml/min/100 gm KW) after HgCl2 (P less than 0.01). In a third group, the RT was increased by a rise of MRPP to 158 +/- 8 mm Hg by bilateral carotid clamping. Subsequently, 3 hours after HgCl2, the GFR decreased not significantly from 72 +/- 6 to 61 +/- 7 ml/min/100 gm KW, and RBF increased from 405 +/- 66 to 431 +/- 71 ml/min/100 gm KW. Three hours of continued carotid clamping alone caused a rise of GFR from 64 +/- 7 to 83 +/- 7 ml/min/100 gm KW (P less than 0.05) and of RBF from 425 +/- 16 to 581 +/- 28 ml/min/100 gm KW (P less than 0.01). Autoregulation of RBF was studied in a control period and after 3 hours of carotid clamping and found to be lost during prolonged carotid clamping. The autoregulatory capacity remained intact after HgCl2 alone. The renal vasoconstrictive response to norepinephrine was not affected 3 hours after carotid clamping. It is concluded that the fall of GFR and RBF after HgCl2 can be prevented by prolonged carotid clamping. This is related to a loss of the capacity to maintain renal vasoconstriction after carotid clamping because of a concomitant loss of autoregulation of RBF and points at least in part to a pathogenetic role of changes in renal hemodynamics in the first hours after HgCl2. The tubular effects of HgCl2 were, however, maintained, despite the protection of GFR.
D058186:Acute Kidney Injury / Q000139:chemically induced / Q000503:physiopathology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002339:Carotid Arteries / Q000502:physiology; D004285:Dogs; D007839:Functional Laterality; D005919:Glomerular Filtration Rate; D006706:Homeostasis; D008627:Mercuric Chloride / Q000494:pharmacology*; D008628:Mercury / Q000032:analysis; D012039:Regional Blood Flow; D012077:Renal Artery / Q000502:physiology; D012079:Renal Circulation / Q000187:drug effects*; D014655:Vascular Resistance / Q000187:drug effects*
D008627:Mercuric Chloride; D008628:Mercury