Md. Garcia et al., HYPOTENSIVE AND HYPERTENSIVE EFFECTS OF CATECHOLAMINES INTRATHECALLY INJECTED IN ANESTHETIZED RATS, Journal of the autonomic nervous system, 59(1-2), 1996, pp. 17-26
The cardiovascular effects of catecholamines intrathecally (i.t.) inje
cted at the T-12-L(1) level were analyzed in pentobarbital anesthetize
d rats. Volumes of injection were not greater than 3 mu l. Noradrenali
ne in doses ranging from 0.03 to 0.3 mu g (i.t.) did not alter the mea
n blood pressure (MBP) while higher doses (1, 3 and 10 mu g, i.t.) cau
sed a dose-dependent increase in MBP. Adrenaline induced hypotensive e
ffects at low doses (0.03-0.3 mu g, i.t.) and presser effects at high
doses (3 and 10 mu g, i.t.). Neither adrenaline nor noradrenaline modi
fied the heart rate. The presser responses to both catecholamines were
antagonized by the alpha(1)-adrenoceptor blocker prazosin (0.05-1 mu
g, i.t.) and by the selective alpha(1A)-adrenoceptor antagonist 5-meth
yl urapidil (10 and 15 mu g, i.t.). In contrast, these presser effects
were not modified by the alpha(1B)-adrenoceptor antagonist chloroethy
lclonidine (90 mu g, i.t.). In animals pretreated with 1 mu g prazosin
(i.t.), low doses of noradrenaline (0.03 and 0.1 mu g, i.t.) caused a
hypotensive effect. Prazosin (1 mu g, i.t.) failed to alter the hypot
ension caused by 0.1 mu g adrenaline. The hypotensive response induced
by either 0.1 mu g noradrenaline (in the presence of prazosin) or 0.1
mu g adrenaline was blocked by the alpha(2)-adrenoceptor antagonist y
ohimbine (1 mg/kg, i.v.), by the GABA-A antagonists bicuculline (3.2 m
u g, i.t.) and picrotoxin (2.7 mu g, i.t.), and by the GABA-B antagoni
st 2-hydroxy saclofen (30 mu g, i.t.). The glycine-receptor antagonist
strychnine (25 mu g, i.t.) did not modify the hypotension induced by
either noradrenaline (in the presence of prazosin) or adrenaline. Thes
e findings suggest that in the low thoracolumbar spinal cord of pentob
arbital-anesthetized rats, noradrenaline and adrenaline have excitator
y as well as inhibitory effects on the control of the BP. The presser
responses of high doses of i.t. injected catecholamines could be media
ted by the activation of spinal alpha(1A)-adrenoceptors, although the
participation of alpha(1B)-adrenoceptors cannot be rule out entirely.
The hypotensive responses induced by low doses of i.t. injected catech
olamines seem to involve the activation of spinal alpha(2A)-adrenocept
ors and the stimulation of an inhibitory GABAergic neuron in the spina
l cord.