S. Guimaraes et al., LACK OF PREJUNCTIONAL AND POSTJUNCTIONAL BETA-ADRENOCEPTOR-MEDIATED EFFECTS IN THE CANINE SAPHENOUS-VEIN AT BIRTH, The Journal of pharmacology and experimental therapeutics, 268(2), 1994, pp. 990-995
The present study was undertaken to compare the relevance of alpha and
beta adrenoceptor-mediated responses at pre- and postjunctional level
in the canine saphenous vein of neonates and adults. To quantify prej
unctional action, the effect of drugs on the neurogenic outflow of tri
tium from the vessel loaded previously with [H-3]norepinephrine or [H-
3]epinephrine was measured. The selective alpha-2 adrenoceptor agonist
UK-14,304 (5-bromo-6-(2-imidazoline-2-ylamino)-quinoxaline: 10-1000 n
M reduced and the selective alpha-2 adrenoceptor antagonist yohimbine
(30-300 nM) enhanced the overflow of tritium evoked by electrical stim
ulation (1 Hz; 2 msec; 100 V; 300 pulses) in both adult and neonate ti
ssues. However, in strips preloaded with [H-3]norepinephrine, the beta
adrenoceptor agonist isoproterenol (50 nM) increased the overflow of
tritium in strips of adults but had no effect in strips of neonates; a
nd in the strips preloaded with [H-3]epinephrine, the beta adrenocepto
r antagonist propranolol (1 mu M) reduced the overflow of tritium in a
dults but had no effect in neonates. Postjunctionally, phenylephrine (
0.1-50 mu M) caused concentration-dependent contractions of the saphen
ous vein rings from adults and neonates but isoproterenol, which cause
d concentration-dependent relaxations on rings contracted previously b
y phenylephrine in adults, had no effect in neonates. In contrast to i
soproterenol, forskolin (0.05-5 mu M), under the same conditions, caus
ed concentration-dependent relaxations of rings of both adults and neo
nates. We conclude that, at birth, there is a lack of pre- and postjun
ctional beta adrenoceptor-mediated responses in canine saphenous vein,
whereas alpha adrenoceptor-mediated responses are fully developed; th
e lack of beta adrenoceptor-mediated responses is due to a failure of
either the receptors or the G proteins, because the directly acting st
imulant of adenylate cyclase forskolin is fully active at that age.