Mechanism of vasopressin-induced increase in intracellular ca2+ ([
ob]ca2+]i) in llc-pk1 porcine kidney cells.
Dibas, Adnan I., S. Mehdi Rezazadeh, Ranga Vassan, Abdul J. Mia, and
Thomas Yorio.
Department of Pharmacology, University of North Texas Health
Science Center at Fort Worth, Fort Worth, TX. 76107, Jarvis Christian
College, Hawkins, TX. 75765
APStracts 3:0339C, 1996.
Analysis of the signal transduction cascade of vasopressin-induced
increase in [Ca2+]i in LLC-PK1 cells was performed. Firstly, a
comparison of the effect of vasopressin on [Ca2+]i in LLC-PK1 cells
to that produced in rat hepatocytes was performed (an intracellular
mobilizing mechanism involving a V1-receptor coupled to the
production of inositol-1,4,5-trisphosphate (IP3)). Secondly, the
effect of known inhibitors of intracellular Ca2+ mobilization on
vasopressin Ca2+-response in LLC-PK1 cells was studied. Vasopressin
induced a transient increase in [Ca2+]i in both LLC-PK1 cells and
hepatocytes. By contrast to the single [Ca2+]i spike seen in LLC-PK1
cells, vasopressin induced an average of two to three [Ca2+]i spikes
in hepatocytes. The V1-antagonist (Pmp1-O-Me-Tyr2-[Arg8]-vasopressin,
1 [mu]M) abolished vasopressin Ca2+-response in both cell-types.
Inhibitors of intracellular Ca2+ mobilization, thapsigargin (5
[mu]M), and U73122 (3 [mu]M) abolished the Ca2+-response by
vasopressin in LLC-PK1 cells. The results suggest that vasopressin
-induced increase in [Ca2+]i in LLC-PK1 cells is mediated via a V1
-like receptor and involves the mobilization of intracellular Ca2+
through an IP3/thapsigargin-sensitive Ca2+-pool.
Received 11 June 1996; accepted in final form 26 September 1996.
APS Manuscript Number C328-6.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 13 November 1996