RELATIONSHIP BETWEEN SYMPATHETIC ACTIVITY AND ARTERIAL-PRESSURE IN CONSCIOUS SPINAL RATS

Spinal cord injury disrupts regulation of arterial pressure, often res ulting in episodic hypertension initiated by spinal reflexes. The cont ribution of spinally generated sympathetic nerve activity (SNA) to con trol of resting arterial pressure after cord injury is questionable. T he mechanisms responsible for the reflex hypertension also are unresol ved. One important question concerns whether or not this hypertension is caused by large spinal sympathetic reflexes or by the known increas ed vascular sensitivity to norepinephrine and limited effectiveness of baroreceptor reflexes that occur after spinal cord injury. We evaluat ed the relationship between renal SNA and mean arterial pressure (MAP) in basal conditions and during reflex presser responses induced by co lon distension in conscious rats for 1 wk after midthoracic spinal cor d transection (SCT). One day after SCT, MAP (69 +/- 6 mmHg) and SNA (6 +/- 2 mu V . s) were lower than the MAP (92 +/- 4 mmHg) and SNA (18 /- 3 mu V . s) in the same anesthetized rats before SCT. At 6 days, MA P increased to 94 +/- 6 mmHg, whereas SNA remained low (4 +/- mu V . s ). One day after SCT, colon distension increased MAP by 28 +/- 4 mmHg and SNA by 35 +/- 6 mu V . s; these responses remained unchanged for 6 days. These data suggest that spinally generated SNA makes no apparen t contribution to basal MAP. In contrast, afferent stimulation can pro duce large excitatory spinal sympathetic reflexes that appear adequate to cause substantial increases in arterial pressure.