IN-VITRO STUDIES OF RELEASE OF ADENINE-NUCLEOTIDES AND ADENOSINE FROMRAT VASCULAR ENDOTHELIUM IN RESPONSE TO ALPHA(1)-ADRENOCEPTOR STIMULATION

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.