Intrathecally administered angiotensin II increases sympathetic activity in the rat

The possibility that angiotensin II (AII) functions as an excitatory transmitter on sympathetic preganglionic neurones was tested in anaesthetized rats. Drugs were administered intrathecally whilst recording blood pressure, heart rate and sympathetic activity in splanchnic or renal nerves. Intrathecal AII (20 microliters, 10(-5) M) caused a significant increase in blood pressure of 13% +/- 3 and in sympathetic activity of 15% +/- 5. Intrathecal AII (20 microliters, 10(-3) M) caused larger increases in blood pressure of 22% +/- 3 and in sympathetic activity of 25% +/- 3. The magnitude of the response was dependent on the location of the catheter tip within the subarachnoid space T9-T11 being best for the above changes. Preceding intrathecal AII with the AII antagonist Saralasin (20 microliters, 10(-3) M) also given intrathecally prevented the changes. An increase in sympathetic nerve activity brought about reflexly by a drop in blood pressure of 45-47 mm Hg was almost halved by intrathecal Saralasin. Peak plasma counts (less than 5% of total) of [3H]AII in the blood after intrathecal injection occurred 2 min after the peak changes in sympathetic activity and blood pressure. Counts of [3H]AII in the spinal cord showed that 81% of recovered label was within one segment on either side of the catheter tip. It is concluded that AII has an excitatory action on sympathetic neurones in the spinal cord.