The resting load-regulated sensitivity of vascular smooth muscle is
mediated by a [ca2+]i-insensitive mechanism.
Miyagi, By Yasushi, Sei Kobayashi, Junji Nishimura, Masashi Fukui, and Hideo
Kanaide.
Division of Molecular Cardiology, Research Institute of Angiocardiology and
Department of Neurosurgery, Neurological institute, Faculty of Medicine,
Kyushu University, Fukuoka, Japan
APStracts 2:0047C, 1995.
The cellular mechanism underlying the regulation of the contraction of
vascular smooth muscles by resting load is unknown. To determine the effects
of changes in the resting load on vascular sensitivity to high K+ and to U
-46619, the force and cytosolic calcium concentration ([Ca2+]i) of
arterial strips were recorded at resting loads of 200mg (optimal load), 50mg
and 10mg. A decrease in the resting load elicited a small decrease in the
basal [Ca2+]i level, without affecting the extent of maximal
[Ca2+]i elevation induced by either stimuli. By decreasing the resting
load, the concentration-response curves for the force development of high K+,
or of U-46619, shifted to the right, while those for [Ca2+]i did not.
We conclude that the basal [Ca2+]i level and the force development, but
not the agonist-induced [Ca2+]i signals, of the vascular smooth muscles
depend on the resting load. We propose that the resting load regulates the
sensitivity of vascular smooth muscles, irrespective of types of stimuli,
through a [Ca2+]i-insensitive mechanism.
Received 10 March 1994; accepted in final form 8 December 1994
APS Manuscript Number C0131-4.
Article publication pending Am. J. Physiol. (Cell Physiology).
ISSN 1080-4757 Copyright 1994 The American Physiological Society.
Published in APStracts on 27 February 1995.