Sodium nitroprusside increases glomerular capillary hydraulic conductivity in isolated rat glomeruli.

Sodium nitroprusside (SNP) causes renal vasodilation, increased renal blood flow, and increased renal sodium excretion. Systemic vascular effects of SNP are dependent on generation of nitric oxide and increase in smooth muscle intracellular cyclic guanosine monophosphate (cGMP). In the current studies isolated glomeruli were used to determine the effects of SNP on glomerular capillary hydraulic conductivity (Lp) and on mesangial tone. The direct effects of the cGMP analogue 8-bromo-cGMP on Lp were studied. Glomeruli were isolated from the superficial renal cortex of adult male Sprague-Dawley rats weighing 143 to 383 gm. Lp was calculated from videomicroscopic images of individual glomeruli during the initial 0.1 second of filtration induced by an albumin oncotic gradient. Incubation of glomeruli in 10(-3) mol/L SNP increased Lp from a control value of 1.38 +/- 0.08 microliter/min.mm Hg.cm2 to 1.91 +/- 0.13 microliter.min.mm Hg.cm2 (p < 0.01). Incubation of glomeruli in 10(-5) mol/L 8-bromo-cGMP increased Lp to a comparable degree from a control value of 2.00 +/- 0.58 microliter/.min.mm Hg.cm2 to 2.39 +/- 0.62 microliter/min.mm Hg.cm2 (p < 0.03). Increase in Lp was observed independent of any effects on systemic or renal circulations, neural effects, or humoral effects. Changes in mesangial tone were estimated from changes in glomerular volume during 15 minutes of incubation with SNP or control medium. Incubation of glomeruli in 10(-5) mol/L SNP increased glomerular volume 6%, a consequence of mesangial relaxation. Incubation of glomeruli in 10(-7) and 10(-3) mol/L SNP did not affect mesangial tone.(ABSTRACT TRUNCATED AT 250 WORDS)