AJP - Regulatory, Integrative and Comparative Physiology, Vol 252, Issue 2 361-R366, Copyright © 1987 by American Physiological Society
Contraction of major artery segments of rat by fish neuropeptide urotensin II
H. Itoh, Y. Itoh, J. Rivier and K. Lederis
Urotensin II (U II) caused marked concentration-dependent contractions of
helical strips from several major arteries of the rat. The thoracic aorta
was most sensitive; the apparent concentration of U II producing
half-maximal contraction was 6.8 X 10(-10) M. Papaverine, dibutyryl cyclic
AMP, forskolin, and nitroprusside antagonized the contractile responses to
U II at the apparent concentrations producing 50% inhibition (IC50) of 7.6
X 10(-6), 2.1 X 10(-4), 2.5 X 10(-6), and 1.5 X 10(-8) M, respectively.
Verapamil, a calcium channel-blocking agent, partially inhibited the
contractile response to U II at IC50 = 6.5 X 10(-6) M. Maximal relaxation,
i.e., a complete inhibition, could not be obtained even at a concentration
of 3 X 10(-5) M verapamil. Cyproheptadine reduced the U II-induced
contraction at higher concentrations. Phentolamine (10(-5) M), propranolol
(10(-5) M), atropine (10(-4) M), tetrodotoxin (10(-6) M), burimamide
(10(-5) M), and indomethacin (10(-5) M) did not change the U II-induced
contraction. At higher concentration, U II (10(-8) M) induced a small
contraction of aortic strips in Ca2+-free Krebs Henseleit solution similar
to that of norepinephrine, but the U II-induced contraction was not
inhibited by phentolamine or propranolol. The action of U II did not
require the presence of endothelial cells. It is concluded that U II acts
on vascular smooth muscle and induces the contraction partly through
intracellular Ca2+ mobilization but mainly by stimulating the influx of
extracellular Ca2+ via potential dependent and potential independent
calcium channels.(ABSTRACT TRUNCATED AT 250 WORDS)
