Central substance P increased blood pressure, heart rate and splanchnic nerve activity in anaesthetized rats without impairment of the baroreflex regulation

In anaesthetized rats the baroreflex was checked before and 15 min after i.c.v. administration of 10 μg SP. The baroreflex was checked indirectly by relating both the reflex prolongation in heart period (inter-beat-interval: IBI) and the reflex inhibition of SNA to a pharmacologically induced BP rise. After i.c.v. administration of SP (n = 10) the resting values of the BP increased significantly from 73 ± 16 mm Hg to 86 ± 9 mm Hg (diastolic pressure) and from 98 ± 20 mm Hg to 113 ± 14 mm Hg (systolic pressure) whilst in the control group (n = 14) the BP remained constant (63 ± 9 vs 63 ± 7 mm Hg diastolic pressure and 106 ± 12 vs 106 ± 9 mm Hg systolic pressure). In the experimental group the resting value in IBI was shortened significantly from 218 ± 40 ms to 167 ± 28 ms (controls: 218 ± 22 ms vs 218 ± 18 ms) and the SNA (estimated in arbitrary units) rose significantly by about 50% in relation to the reference period before i.c.v. SP (3.31 ± 0.11 vs 6.27 ± 0.17 arbitrary units per IBI). In contrast, the baroreflex behaved similarly before and after any treatment, i.e. both the reflex prolongation in IBI (1.34 ± 0.75 vs 1.39 ± 0.95 ms/mm Hg) and the reflex inhibition of SNA (0.0312 ± 0.01 vs 0.0555 ± 0.015 arbitrary units/mm Hg) caused by that pharmacologically induced BP rise were comparable before and after i.c.v. SP. These results indicate that the baroreflex operates at a different operating point but without impairment in the baroreflex sensitivity after i.c.v. administration of SP.