From the Department of Physiology, Faculty of Medicine, Tabriz University of Medical Sciences, Tabriz, I.R. Iran
Abstract: (4813 Views)
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) producd
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.