Clonidine causes dilatation of the aorta in the presence of endothelium, wh
ile it causes contraction of the aorta in the absence of endothelium. The p
resent study was carried out to clarify the role of alpha-1-adrenoceptors i
n the vascular action of clonidine. The aortic rings were suspended in Kreb
s-Henseleit (K-H) medium, and the effects of alpha-1- and alpha-2-adrenocep
tor antagonists on the clonidine-induced contractions were measured. Moreov
er, the role of the phosphatidylinositol (PI) response was examined. The ao
rtic slices were incubated in K-H medium containing, [H-3]myo-inositol and
clonidine. The formation of [H-3]inositol monophosphate (IP1) was measured
with a liquid scintillation counter.
Clonidine caused contraction of the aorta in the absence of endothelium, in
a dose-dependent manner. This contraction was inhibited by antagonists in
the following order of the potency: prazosin > phentolamine > spiperone > u
rapidil = yohimbine > L-659066 > atipamezole. On the other hand, clonidine
inhibited norepinephrine (NE)-induced contraction in the aorta in the absen
ce and in the presence of endothelium. Clonidine enhanced IP1 accumulation
in the aorta in the absence of endothelium, whereas it inhibited NE-induced
IP1 accumulation in the aorta.
The present results show that alpha-1-adrenoceptors are probably involved i
n the clonidine-induced contraction and relaxation of the rat aorta.