AJP - Renal Physiology, Vol 253, Issue 2 328-F332, Copyright © 1987 by American Physiological Society
Vasopressin increases cytosolic free calcium in LLC-PK1 cells through a V1-receptor
M. A. Burnatowska-Hledin and W. S. Spielman
We examined the effects of arginine vasopressin (AVP), parathyroid hormone
(PTH), and bradykinin (BK) on the cytosolic free calcium concentration
([Ca]i) in cultured LLC-PK1 and MDCK kidney cell lines by use of the
fluorescent Ca chelator fura-2. In LLC-PK1 cells, the addition of AVP but
not [1-desamino-8-D-arginine]vasopressin (dDAVP, V2 agonist), PTH, or BK
(10(-6) M) caused a significant increase in [Ca]i. The AVP-induced increase
in [Ca]i from 61 +/- 6 to 225 +/- 44 nM (n = 7, P less than 0.01) was rapid
and transient, returning to base line in 2 to 3 min. The effect of AVP was
dose dependent and was present at 1 (61% increase) but not 5 min after
extracellular Ca was removed. The effect of 10(-6) M AVP could be blocked
with the pressor (V1) antagonist, d(CH2)5Tyr(Me)AVP, but not dDAVP. In MDCK
cells, BK, but not AVP and PTH, increased [Ca]i from 146 +/- 11 to 281 +/-
31 nM (n = 9, P less than 0.001). The removal of extracellular Ca (5 min),
reduced but did not abolish this effect. These results indicate that [Ca]i
mobilized by activation of V1-receptors may mediate AVP-regulated function
in some transporting epithelia.
