AJP - Renal Physiology, Vol 252, Issue 1 115-F121, Copyright © 1987 by American Physiological Society
Calcium modulates vasopressin effect in rabbit cortical collecting tubule
M. A. Dillingham, B. S. Dixon and R. J. Anderson
The calcium ion has been proposed to be an important mediator of the
hydroosmotic response to arginine vasopressin (AVP). We examined the effect
of reducing basolateral calcium activity on hydraulic conductivity (Lp) in
response to AVP in rabbit cortical collecting tubules (CCT) perfused in
vitro. Each tubule served as its own control. Reducing bathing fluid
calcium from 0.94 mM to 4.6 microM reduced Lp in each tubule (mean decrease
from 146 +/- 13 to 106 +/- 7 cm X s-1 X atm X 10(-7), n = 11, P less than
0.025). To determine whether this inhibitory effect was due to a decrease
in cellular calcium uptake, we measured the effect of adding 10(-4) M
lanthanum to bathing fluid on AVP-stimulated Lp. Lanthanum decreased Lp
(from 109 +/- 13 to 80 +/- 10 cm X s-1 X atm X 10(-7), P less than 0.05) in
each tubule. To examine the site at which low peritubular calcium activity
regulates AVP action, we measured the effect of decreasing bathing fluid
calcium on 8-[p-chlorophenylthio]-adenosine 3',5'-cyclic monophosphate
(ClPheS-cAMP)-stimulated Lp (n = 5). Decreasing bathing fluid calcium
significantly decreases (P less than 0.025) Lp response to ClPheS-cAMP.
Since these results suggest that cellular calcium uptake can exert a
post-cAMP effect to modulate AVP action, we examined the effect of the
calcium ionophore A23187 (10(-7) M) on AVP- and ClPheS-cAMP-stimulated Lp
A23187 reversibly potentiates (25-30%, P less than 0.025) the Lp response
to both AVP and ClPheS-cAMP.(ABSTRACT TRUNCATED AT 250 WORDS)
