SPINAL-CORD REGULATION OF SYMPATHETIC ACTIVITY IN INTACT AND SPINAL RATS

Excitatory amino acid (EAA) and cholinergic neurotransmission in the s pinal cord of urethan-anesthetized rats was investigated to assess mec hanisms regulating sympathetic activity after spinal cord injury. Bloc kade of EAA transmission by intrathecal injection of kynurenic acid de creased arterial blood pressure by 24 +/- 4 mmHg, heart rate by 15 +/- 10 beats/min, and renal sympathetic nerve activity (RSNA) by 85 +/- 4 % in intact rats. In rats with cervical spinal transections, this bloc kade decreased RSNA by 51 +/- 5% and had no effect on arterial pressur e and heart rate. Muscarinic blockade by intrathecal atropine decrease d BSNA by 12 +/- 3 and 32 +/- 6% in intact and spinal rats, respective ly, and caused no cardiovascular responses in either group. Combined b lockade of EAA and muscarinic receptors in spinal rats decreased RSNA by 77 +/- 1%. Intrathecal injections of the EAA agonist D,L-homocystei c acid in spinal rats caused initial increases (335 +/- 28%) in RSNA l asting similar to 3 min and later sustained increases (157 +/- 19%) la sting 36 +/- 8 min. Only the early excitation increased arterial press ure by 17 +/- 3 mmHg, and then pressure returned to baseline values. T he EAA agonist kainic acid increased RSNA by 402 +/- 90% in spinal rat s, an effect lasting 70 +/- 5 min, and increased arterial pressure by only 8 +/- 2 mmHg for 12 +/- 5 min. These findings suggest that tonic activity of spinal neurons with EAA and cholinergic receptors maintain s tonic RSNA after spinal cord transection. However, this activity doe s not play a major role in maintaining arterial pressure, even if it i s increased substantially by EAA receptor stimulation.