Oxygen induces electromechanical coupling in arteriolar smooth
muscle cells: arole for l-type ca2+ channels.
Welsh, Donald G., William F. Jackson, and Steven S. Segal.
John B. Pierce Laboratory and Department of Cellular and Molecular
Physiology, Yale University School of Medicine, New Haven,
Connecticut 06519
APStracts 5:0084H, 1998.
We tested whether O2-induced vasomotor responses of arterioles
correspond to changes in membrane potential (Em) of cells in the
arteriolar wall. The cheek pouch of anesthetized male hamsters was
prepared for intravital microscopy and intracellular recording.
Microelectrodes containing Lucifer yellow dye were used to label
smooth muscle cells (SMCs) or endothelial cells (ECs) during
arteriolar responses to O2. When superfused with low PO2 ( 20 torr;
arteriolar diameter, 55 ( 2 (m), Em of SMCs and ECs averaged -37 and
-36 mV, respectively. Superfusion with high PO2 ( 150 torr)
depolarized SMCs (to -15 ( 1 mV) with vasoconstriction (to 24 ( 2 (m)
and diameter cycled with Em of SMCs during vasomotion. In contrast,
Em of ECs did not change with PO2 nor during vasomotion, yet
depolarized by 21 ( 2 mV when extracellular K+ ([K+]o) was raised to
55 mM. Superfusion with diltiazem (10 [mu]M) or nifedipine (1 [mu]M)
abolished vasomotor and electrical responses to PO2 in SMCs but not
depolarizations to elevated [K+]o. We conclude that, under
physiological conditions, electrical and mechanical responses of
arteriolar SMCs to changes in PO2 are mediated through L-type Ca2+
channels without corresponding electrical activity in ECs.
Received 22 December 1997; accepted in final form 13 February
1998.
APS Manuscript Number H1167-7.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1998 The American Physiological Society.
Published in APStracts on 9 March 1998