en Physiology Physiology Original Research: Basic Science in Medicine Original Research: Basic Science in Medicine The selective a2 -adrenoceptor agonist UK-14304 produces a small vasoconstrictor response in the rat isolated carotid artery. The purpose of the work presented here was to investigate whether stimuli that produce submaximal contraction would potentiate responses to UK-14304. Male Wistar rats were killed by overdose with pentobarbitone sodium, after which the left and right common carotid arteries were removed. The rings of arteries 3-4 mm in length were cut from each vessel and then mounted in 10 mL isolated organ bath, bathed in Krebs maintained at 37°C and gassed with 95% 02 plus 5% CO2, The preparations were allowed to equilibrate for an hour. Cumulative concentration-response curves (CCRC) were constructed in a cumulative manner by increasing the concentration of the agonists in half-log increments. When antagonists were used, the preparations were incubated at least for 45 minutes with the drugs prior to the onset of a second CCRC. Angiotensin II (All) and other contracting factors were added approximately 10-15 min prior to the onset of CCRC to an agonist. After inducing tone with low concentrations of the thromboxane A2 mimetic agent U-46619 (lnM), 5HT (0.5-1 ).lM) and phenylephrine (l0 nM), exposure of the preparation to UK-14304 resulted in concentration dependent conWrctions to this agonist. The sensitivity and maximum response of the preparation ,to' UK-14304 were not changed. Inducing tone with All (0.01 µM) produc􀁶d a significant leftward shift in the CCRC to UK-14304 (p<0.05). Thus submaximal contraction with All (0.01 µ M) increased responses significantly, but inducing tone with phenylephrine, U-46619 and 5HT had no effect on responses to UK-14304. The α-adrenoceptor antagonists prazosin and rauwolscine were examined to see whether UK-14304's main action in the presence of All remained via al. The potentiated responses were . prazosin sensitive and rauwolscine resistant, indicating an increasing effect mediated by al-adrenoceptors. α-adrenoceptors, UK-14304, prazosin, rauwolscine, angiotensin II 83 88 http://mjiri.iums.ac.ir/browse.php?a_code=A-10-298-263&slc_lang=en&sid=1 M MOHAMMADI NAGHADEH 20031947532846004182 20031947532846004182 Yes From the Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, I.R. Iran JC McGRATH 20031947532846004183 20031947532846004183 No the Clinical Research Initiative in Heart Failure, West Medical Building, University of Glasgow, Glasgow G21-BQQ, Scotland.