Evidence for contribution of effector organ cellular responses to
the biphasic dynamics of heat acclimation.
Horowitz, Michal, Pavel Kaspler, Yithak Marmari, and Yoram Oron.
Division of Physiology and Department of Radiology, Hadassah
Schools of Medicine and Dental Medicine, The Hebrew University,
Jerusalem and Department of Physiology and Pharmacology, Sackler
School of Medicine, Tel-Aviv University, Israel
APStracts 2:0392A, 1995.
The involvement of cellular processes in the biphasic dynamics of heat
acclimation was studied. Key steps in the cholinergic signal
transduction pathway for water secretion were measured in
submaxillary gland of acclimating (2 days-STHA and 30 days-LTHA at
34_C) or acute heat stressed (HS, 2 h at 40_C) rats in vitro. Both
the carbamylcholine (CCh)-induced maximal fractional rate (Vmax) and
the total 86Rb+ efflux, reflecting K+ efflux and water transport,
transiently decreased (p<0.001) on STHA. Upon LTHA, the total K+
efflux increased (p<0.001), while Vmax increased only slightly.
During STHA, the density of the high affinity binding site of the
muscarinic receptors (MR) increased by 50% and their affinity for the
muscarinic antagonist 3H-NMS decreased transiently by 87%. Basal
cytosolic [Ca2+]i decreased (p<0.05), but the peak CCh-induced
[Ca2+]i increase resembled the controls. Upon LTHA, MR density
continued to increase (100%, p<0.05) while affinity resumed
control values. Basal and CCh-induced [Ca2+]i increase returned to
control levels. We conclude that glandular cellular processes follow
a biphasic pattern with major apparent changes attributable to events
distal to the [Ca2+]i rise. This was further validated by employing
HS which produced qualitatively different effects on the MR profile,
with a decrease in 86Rb+ efflux comparable to STHA. Hence, although
heat-induced changes in the proximal components of the signal
transduction pathway may contribute to altered regulatory span, the
predominant apparent cellular effect is on the distal part of the
pathway.
Received 9 June 1995; accepted in final form 29 August 1995.
APS Manuscript Number A611-5.
Article publication pending Journal of Applied Physiology.
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 23 September 1995.