K. Shinozuka et al., IN-VITRO STUDIES OF RELEASE OF ADENINE-NUCLEOTIDES AND ADENOSINE FROMRAT VASCULAR ENDOTHELIUM IN RESPONSE TO ALPHA(1)-ADRENOCEPTOR STIMULATION, British Journal of Pharmacology, 113(4), 1994, pp. 1203-1208
1 Noradrenaline-induced release of endogenous adenine nucleotides (ATP
, ADP, AMP) and adenosine from both rat caudal artery and thoracic aor
ta was characterized, using high-performance liquid chromatography wit
h fluorescence detection. 2 Noradrenaline, in a concentration-dependen
t manner, increased the overflow of ATP and its metabolites from the c
audal artery. The noradrenaline-induced release of adenine nucleotides
and adenosine from the caudal artery was abolished by bunazosin, an a
lpha(2)-adrenoceptor antagonist, but not by idazoxan, an alpha(2)-adre
noceptor antagonist. Clonidine, an alpha(2)-adrenoceptor agonist, cont
racted caudal artery smooth muscle but did not induce release of adeni
ne nucleotides or adenosine. 3 Noradrenaline also significantly increa
sed the overflow of ATP and its metabolites from the thoracic aorta in
the rat; however, the amount of adenine nucleotides and adenosine rel
eased from the aorta was considerably less than that released from the
caudal artery. 4 Noradrenaline significantly increased the overflow o
f ATP and its metabolites from cultured endothelial cells from the tho
racic aorta and caudal artery. The amount released from the cultured e
ndothelial cells from the aorta was also much less than that from cult
ured endothelial cells from the caudal artery. In cultured smooth musc
le cells from the caudal artery, a significant release of ATP or its m
etabolites was not observed. 5 These results suggest that there are va
scular endothelial cells that are able to release ATP by an alpha(1)-a
drenoceptor-mediated mechanism, but that these cells are not homogeneo
usly distributed in the vasculature.