POLYCATION-INDUCED DISLOCATION OF SLIT DIAPHRAGMS AND FORMATION OF CELL JUNCTIONS IN RAT-KIDNEY GLOMERULI - EFFECTS OF LOW-TEMPERATURE, DIVALENT-CATIONS, COLCHICINE, AND CYTOCHALASIN-B

  • 1 January 1978
    • journal article
    • research article
    • Vol. 39  (5) , 430-440
Abstract
Neutralization of negatively charged groups in the glomerular capillary wall by polycations causes extensive loss of podocyte footplates, formation of tight and gap junctions and dislocation of slit diaphragms within a few min. The development of podocyte abnormalities was further evaluated by quantitating the effects of inhibitors of microfilaments, microtubules and cellular metabolism. The decrease in the number of footplates per .mu.m of basement membrane caused by the polycationic chemical protamine sulfate (PS) was determined after in situ perfusion of the left kidney of rats. An approximate 50% amelioration of this effect of PS was observed when in addition to perfusion with PS:perfusion was performed in the cold (6.degree. C.); the perfusate contained cytochalasin B; the perfusate lacked Ca2+; and the perfusate contained EDTA. Colchicine did not affect PS-induced footplate loss. The PS-induced footplate retraction observed in scanning micrographs, is partially an active process involving podocyte actin filaments. Intact microtubuli are not necessary. Formation of tight and gap junctions between foot processes and dislocation of slit diaphragms were not influenced by any of the inhibitory conditions listed above.