Histochemical Alterations Revealed by Tetrazolium Chloride in Hypertensive Kidneys in Relation to Renal VEM Mechanisms. ∗

Abstract

Summary and conclusions

The incubation of slices of renal cortex with tetrazolium chloride (TTC) has disclosed patterns of formazan deposition in the proximal convoluted tubules with striking differences between normal and hypertensive kidneys obtained from dogs, rats and man. In the proximal convoluted tubules of kidneys from normotensive animals and man, the formazan is deposited as fine dust-like granules evenly distributed within the cytoplasm. In the hypertensive kidney the formazan is deposited in coarse clumps, plaques or needles, commonly at the cell margins and often extracellularly as well.

Despite the difference in formazan patterns the total amount of reduced TTC per mg of kidney tissue is approximately the same in normal and hypertensive kidneys, as is the oxygen consumption determined by the conventional micro-respiration technic. Concurrent studies of VEM metabolism show the uniform restriction of VEM production to anaerobiosis in normal kidneys, and the formation of VEM under both anaerobic and aerobic conditions by the hypertensive kidneys of animal and human subjects. When the VEM metabolism of a kidney from a normotensive rat, dog or human is transformed to the hypertensive type by a period of prior anaerobiosis in vitro, there is a parallel development of the characteristic hypertensive formazan pattern in the proximal convoluted tubules.

The reduction of TTC to the insoluble formazan results from an interaction between TTC and enzyme systems within the cell. The observations reported would indicate some alteration in the metabolic characteristics of the proximal convoluted tubules in experimental renal and essential hypertension. The association of these histochemical changes in the proximal convoluted tubules with alterations of the VEM mechanisms in experimental and human hypertension suggests, 1) that the proximal tubules may be the site of VEM formation, and 2) that the failure of the hypertensive kidney to limit VEM formation to anaerobiosis may be related to the enzymatic disorganization revealed by TTC.

Finally, the data presented provide specific evidence for a similarity between experimental renal hypertension and essential hypertension in man.