Platelet-activating factor attenuates the arginine vasopressin-induced fall of transepithelial resistance across inner medullary collecting duct monolayers.

  • 1 January 1992
    • journal article
    • Vol. 18  (1) , 9-14
Abstract
Platelet-activating factor (PAF) is a vasoactive substance produced in the medulla which may alter Na excretion by the kidney. To examine a possible site and mechanism of action of PAF on the kidney, we evaluated the effects of PAF on transepithelial resistance and intracellular calcium concentration ([Ca2+]i) in cultured rat inner medullary collecting duct cells. Exposure of inner medullary collecting duct (IMCD) cell monolayers to PAF had no significant effect on basal transepithelial resistance. By contrast, incubation of IMCD cells with PAF reversibly blocked the fall in transepithelial resistance induced by arginine vasopressin (AVP): -11.1 +/- 1.4 omega.cm2 with AVP versus -0.02 +/- 1.6 omega.cm2 with PAF and AVP. Exposure of IMCD cells to PAF in Ca-replete medium caused a rise in intracellular calcium from 155 +/- 25 to 491 +/- 68 nM. By contrast, exposure of IMCD cells to PAF in Ca-free medium produced no change in [Ca2+]i. Because the rise in [Ca2+]i induced by PAF was absent in Ca-free medium, transepithelial resistance across IMCD monolayers was examined in calcium-free medium. The effect of PAF to block the fall in transepithelial resistance induced by AVP was maintained in Ca-free medium. These data suggest that PAF modulates the effect of AVP on conductive channels by a mechanism distinct from changes in intracellular calcium.

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