People with high level
spinal cord injury (SCI) suffer from both
hypotension and spontaneous
hypertension due to loss of supraspinal control of spinal sympathetic outflow. Few reports have addressed whether any changes occur in central regulation of blood pressure (BP) and heart rat (HR) at the supraspinal level. Central
tachykinin NK-1 and
NK-3 receptors are located in many cardiovascular areas in the brain and are known to modulate BP and HR. This study examined the intracerebroventricular (i.c.v.) effects of the selective
NK-1 receptor agonist [Sar(9), Met(O(2))(11)]SP (65pmol, n=6) and
NK-3 receptor agonist
senktide (650pmol, n=6) on mean arterial pressure (MAP) and HR before and after complete
spinal cord transection at thoracic level 4 (T4). [Sar(9), Met(O(2))(11)]SP evoked increases in MAP and HR which were still present 4days after the T4 SCI. Further analysis using the beta(1)-adrenoceptor antagonist
atenolol (10mgkg(-1)) revealed an increased contribution of HR in the MAP increase after SCI. For
senktide, 2 and 5weeks after T4 SCI, the rise in MAP induced by
senktide was significantly increased in magnitude and was similar to a normal response at 8weeks. These effects were accompanied by a
bradycardia, which was still present and amplified at 8weeks. Our results reveal a transient potentiation of the
senktide-mediated MAP effect and a greater contribution of the HR in MAP increase by [Sar(9), Met(O(2))(11)]SP in T4 transected rats. Although the significance of these changes remains to be established. This suggest a reorganization of supraspinal mechanisms regulating BP and HR after a high level SCI. Central NK-1 and
NK-3 receptors might therefore contribute to the maintenance of MAP following high thoracic SCI.