Spinal cord injury disrupts regulation of arterial pressure, often resulting in episodic hypertension initiated by spinal reflexes. The contribution of spinally generated sympathetic nerve activity (SNA) to control of resting arterial pressure after cord injury is questionable. The mechanisms responsible for the reflex hypertension also are unresolved. One important question concerns whether or not this hypertension is caused by large spinal sympathetic reflexes or by the known increased vascular sensitivity to norepinephrine and limited effectiveness of baroreceptor reflexes that occur after spinal cord injury. We evaluated the relationship between renal SNA and mean arterial pressure (MAP) in basal conditions and during reflex pressor responses induced by colon distension in conscious rats for 1 wk after midthoracic spinal cord transection (SCT). One day after SCT, MAP (69 +/- 6 mmHg) and SNA(6 +/- 2 microV x s) were lower than the MAP (92 +/- 4 mmHg) and SNA (18 +/- 3 microV x s) in the same anesthetized rats before SCT. At 6 days, MAP increased to 94 +/- 6 mmHg, whereas SNA remained low (4 +/- 1 microV x s). One day after SCT, colon distension increased MAP by 28 +/- 4 mmHg and SNA by 35 +/- 6 microV x s; these responses remained unchanged for 6 days. These data suggest that spinally generated SNA makes no apparent contribution to basal MAP. In contrast, afferent stimulation can produce large excitatory spinal sympathetic reflexes that appear adequate to cause substantial increases in arterial pressure.
- Copyright © 1997 the American Physiological Society