Memory of arterial receptor activation involves reduced [ca2+[ cb]i
and desensitization of crossbridges to [ca2+]i.
Ratz, Paul H., Frank A. Lattanzio, Jr, and Paul-Michael Salomonsky.
Department of Pharmacology, Eastern Virginia Medical School, P.O.
Box 1980, Norfolk, VA 23501
APStracts 2:0240C, 1995.
Rabbit femoral arteries retain a memory of previous maximum receptor
activation for up to 3-4 h after complete cessation of the stimulus,
as reflected by a reduction in the steady-state contraction produced
by a subsequent exposure to KCl. The present study examined the
hypothesis that this modulatory effect involves alterations in post
-receptor signal transduction. To quantify the degree of cellular
down-regulation induced by an episode of 1-adrenoceptor stimulation,
tissues were pretreated for 30 min with 10-5 M PhE, washed for 10 min
to cause complete relaxation and activated with increasing
concentrations of KCl. Pretreatment of tissues with PhE resulted in a
large reduction compared to control tissues in the ability of 20-60
mM KCl to increase stress and MLC phosphorylation. However, only at
low (20 and 26 mM), but not high (>26 mM) KCl concentrations did
PhE pretreatment reduce the ability of KCl to increase [Ca2+]i. These
data support the hypothesis that memory of receptor activation
involves reductions in both Ca2+-mobilization and the sensitivity of
contractile proteins to [Ca2+]i.
Received 27 February 1995; accepted in final form 15 June 1995.
APS Manuscript Number C107-5.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 11 July 1995.