Neural and humoral mechanisms involved in the generation of arterial pressure lability in rats.

1. The role of the renin-angiotensin system (RAS) and sympathetic nervous system (SNS) in the generation of the arterial pressure lability (APL) observed after sino-aortic deafferentation (SAD) in rats was evaluated. 2. SAD was performed in normotensive (N = 8), renal hypertensive (2K-1C, N = 8) and spontaneously hypertensive rats (SHR, N = 8) and mean arterial pressure (MAP) recordings were performed 24 h after SAD. 3. MAP was recorded by a computerized technique using a sampling frequency of 30 Hz for 30 min and the data obtained were used to calculate APL. After MAP measurements the activity of the RAS and SNS was pharmacologically evaluated in all groups by the changes in MAP in response to iv injection of captopril and hexamethonium chloride, respectively. 4. SAD produced an increase in MAP (118 +/- 4 vs 99 +/- 2 mmHg) and a large increase in APL (13.4 +/- 1.3 vs 3.8 +/- 0.3 mmHg) in normotensive rats. SAD produced no changes in MAP (161 +/- 7 vs 167 +/- 7 mmHg) in 2K-1C hypertensive rats but induced a large increase in APL (6.7 +/- 0.5 vs 12 +/- 1 mmHg). SAD also produced no changes in MAP (152 +/- 3 vs 152 +/- 4 mmHg) in SHR but induced a marked increase in APL (6.7 +/- 0.3 vs 21 +/- 2.3 mmHg). 5. All SAD rats presented a larger fall in MAP in response to captopril and hexamethonium than the respective control group with intact baroreceptors suggesting an overactivity of both systems after SAD in normotensive, renal hypertensive and spontaneously hypertensive rats. 6. The data also show that SAD produced no additional increase in MAP but promoted a significant increase in APL in renal and spontaneously hypertensive rats. 7. We suggest that APL observed after SAD in different experimental models is dependent on an interaction of RAS and SNS, both of which seem to be overactive after removal of arterial baroreceptors.