Glomerular hemodynamics in mercury-induced acute renal failure

Glomerular hemodynamics in mercury-induced acute renal failure. As manifest by tubular collapse and the virtual absence of flow into the glomerulotubular junction (GTJ), filtration in most nephrons (SNGFR) of rats poisoned with 9 mg/kg body wt HgCl2 16 to 28 hours earlier was virtually absent. Arterial colloid osmotic pressure (COPA) and Bowman's space pressure (PBS) were modestly depressed (P < 0.05 or below), and mean blood pressure was reduced from 115 ± 2 mm Hg (SEM) to 97 ± 1 mm Hg (P < 0.001). Glomerular capillary hydraulic pressure (Pg), 25.6 ± 1.3 mm Hg was some 24 mm Hg lower than control (P < 0.001) and yielded a net afferent effective filtration pressure (Pnet) of 4.1 ± 1.2 mm Hg. Excluding three rats with values greater than 10 mm Hg, Pnet averaged 2.0 ± 0.9 mm Hg (N = 17 rats) versus 20.0 ± 1.8 mm Hg in controls (N = 10, P < 0.001), the former being statistically almost indistinguishable from 0 mm Hg and barely able to support any filtration. This decrease in Pg was caused by a major increase in preglomerular resistance (RA) and a reciprocal fall in efferent arteriolar resistance (RE), the RA/RE ratio of 7.2 ± 0.8 being fourfold higher than control (P < 0.001). Renocortical blood flow was not different from control (P > 0.2). A wide spread of Pg values in individual glomeruli and the absence of tubular flow despite the appearance of i.v. injected lissamine green in a quadrant of surface glomeruli suggested the possibility of a greatly increased, glomerular capillary resistance. It is concluded that reciprocal changes in RA and RE are the immediate cause of filtration failure in this form of ARF and that, in the virtual absence of filtration, tubular leakage can play no important role. Since PBS was depressed in both the developmental and established phases of ARF, tubular obstruction appears to play no direct role in the pathogenesis of this particular model of murine acute renal failure.