Key result
Spinal excitatory and cholinergic receptors maintain RSNA but not arterial pressure following spinal cord transection.
Why the study?
Mechanisms regulating sympathetic activity after spinal cord injury involving excitatory amino acid and cholinergic neurotransmission in the spinal cord were investigated.
Population
Urethan-anesthetized intact rats and rats with cervical spinal transections
Comparison
Intrathecal injection of kynurenic acid, atropine, D,L-homocysteic acid, or kainic acid
Design
Preclinical experimental study
Authors
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Does not support spinal excitatory or cholinergic blockade to maintain arterial pressure after transection; leaves open their contribution to renal sympathetic activity in injury models.
Tonic activity of spinal neurons with EAA and cholinergic receptors maintains tonic renal sympathetic nerve activity after spinal cord transection, but does not play a major role in maintaining arterial pressure.
Hong et al. (1994) studied Spinal cord injury. Intrathecal injection of kynurenic acid, atropine, D,L-homocysteic acid, or kainic acid was evaluated on Renal sympathetic nerve activity (RSNA), arterial blood pressure, and heart rate. Tonic activity of spinal neurons with excitatory amino acid and cholinergic receptors maintains tonic renal sympathetic nerve activity after spinal cord transection but does not maintain arterial pressure.
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