HYPOTENSIVE AND HYPERTENSIVE EFFECTS OF CATECHOLAMINES INTRATHECALLY INJECTED IN ANESTHETIZED RATS

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.