Endothelial inhibition of myofilament calcium response in intact
cardiac myocytes.
Pepper, Chris B., Derek Lang, Malcolm J. Lewis, and Ajay M. Shah.
Departments of Cardiology and Pharmacology, University of Wales
College of Medicine, Cardiff, U.K.
APStracts 2:0194H, 1995.
Recent studies suggest that factors released by endothelial cells can
modify contraction of isolated cardiac preparations. We compared the
effects of (i) coronary effluent collected from Langendorff-perfused
rat hearts and (ii) cultured vascular endothelial cell superfusate on
isolated fura-2-loaded rat ventricular cardiac myocytes. Coronary and
cultured cell effluent produced similar effects. Isotonic contraction
amplitude was reduced by 31.6+/-2.6% and 70.2+/-9.1% respectively;
myocyte diastolic length increased by 0.8+/-0.2[mu]m and 1.5+/
-0.4[mu]m, and time to 50% relaxation fell by 6.2+/-1.8% and 10.1+/
-2.0% (all p<0.05, n=29 and 15). A small fall in the amplitude of
the intracellular Ca2+ transient was observed (8.5+/-1.5%, 10.9+/
-3.5%, both p<0.01), insufficient to account for the reduction in
twitch amplitude. In intact myocytes tetanized in the presence of
thapsigargin, the steady state myofilament response to Ca2+ was
reduced by coronary and cultured cell effluent. These results suggest
that both coronary endothelial cells in situ and cultured endothelial
cells tonically release a factor(s) that reduces myofilament Ca2+
response.
Received 22 August 1994; accepted in final form 24 April 1995.
APS Manuscript Number H759-4.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1995 The American Physiological Society.
Published in APStracts on 16 May 1995.