Contractile actions of c5a on isolated porcine coronary resistance
and conductance arteries.
Rendig, Stephen V., Sarah Gray, Ezra A. Amsterdam.
Division of Cardiovascular Medicine, Department of Internal
Medicine and Department of Human Physiology, School of Medicine,
University of Californiam Davis, California 95616
APStracts 3:0274H, 1996.
The comparative effects of the complement component, C5a, on coronary
resistance and conductance arteries have not been evaluated. To
clarify the coronary contractile actions of this anaphylatoxin, we
studied the effects of C5a on development of isometric tension in
isolated porcine coronary conductance and resistance arteries.
Internal diameters of conductance and resistance vessels were 367 +/-
21 and 88 +/- 4 [mu]m, respectively. Vessel ring segments were
suspended in a microvessel myograph, stretched to the peaks of their
length-tension curves and precontracted with 30 mM K+ physiological
salt solution. Dose-response curves to C5a (2, 10, 50 nM) were
obtained. At 50 nM, the C5a-induced increase in tension in resistance
arteries (4.1 +/- 0.9 to 5.7 +/- 1.4 mN, 35.8 +/- 3.4%) was
significantly greater (p < 0.05) than in conductance arteries
(10.7 +/- 2.2 to 12.4 +/- 2.6?mN, 15.6 +/- 3.0%). A specific
thromboxane A2 receptor antagonist, SQ 29,548, virtually eliminated
C5a-induced increases in tension. C5a did not impair endothelium
-dependent relaxation in either conductance or resistance vessels, as
indicated by ED50 calculated from bradykinin dose-response curves
before and after exposure of the vessels to 50 nM C5a (Resistance:
pre-C5a ED50 = 2 nM, post-C5a ED50 = 3 nM; conductance: pre-C5a ED50
= 13 nM, post-C5a ED50 = 14 nM). These results indicate that 1) C5a
has a greater vasoconstrictive effect on isolated porcine resistance
than conductance coronary arteries; 2) C5a-induced coronary
constriction is mediated by thromboxane A2; and 3) C5a does not
impair endothelium-dependent relaxation of isolated porcine coronary
arteries.
Received 16 January 1996; accepted in final form 20 June 1996.
APS Manuscript Number H29-6.
Article publication pending Am. J. Physiol. (Heart Circ. Physiology).
ISSN 1080-4757 Copyright 1996 The American Physiological Society.
Published in APStracts on 25 July 1996