Effect of elevated interstitial pressure on the renal cortical hemodynamics.
The influence of renal interstitial pressure on the resistance pattern within the superficial cortical vasculature has been investigated from determinations of 1) the glomerular blood flow eith a modified microsphere technique and 2) the intravascular hydrostatic pressures. Interstitial pressure was monitored via a 50 mum PVC-catheter placed into the subcapsular interstitial space. Two conditions were analyzed viz. a) elevation of uretheral pressure to 20 mm Hg and b) venous stasis to 10-15 mm Hg. Both conditions produced an increase in the interstitial pressure from 1-2 mm Hg to about 5 mm Hg as well as an increased hilar lymph flow and protein flow of about the same size. The vascular reactions were different, however. Uretheral stasis (but not the stasis of a single nephron) produced a decreased resistance in the afferent arteriolae with a concomitant increae in the pressures in the glomerular capillaries, and the peritobular capillary network. In contrast, venous stasis produced only small changes in the parameters studied but for the obvious rise in the peritubular capillary pressure. The results suggest that factors other than the interstitial pressure are governing the afferent vascular tone; the tubular wall tension might be one of these factors.
D000818:Animals; D001794:Blood Pressure; D002200:Capillary Resistance; D005110:Extracellular Space; D005919:Glomerular Filtration Rate; D006874:Hydrostatic Pressure; D007672:Kidney Cortex / Q000098:blood supply*; D007678:Kidney Glomerulus / Q000098:blood supply*; D007684:Kidney Tubules / Q000098:blood supply*; D008196:Lymph / Q000378:metabolism; D008297:Male; D051381:Rats; D012082:Renal Veins / Q000502:physiology; D014521:Urethra / Q000502:physiology