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 nerv ous system (SNS) in the generation of the arterial pressure lability ( APL) observed after sine-aortic deafferentation (SAD) in rats was eval uated. 2. SAD was performed in normotensive (N = 8), renal hypertensiv e (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 fre quency of 30 Hz for 30 min and the data obtained were used to calculat e APL. After MAP measurements the activity of the RAS and SNS was phar macologically evaluated in all groups by the changes in MAP in respons e to iv injection of captopril and hexamethonium chloride, respectivel y. 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 normote nsive rats. SAD produced no changes in MAP (161 +/- 7 vs 167 +/- 7 mmH g) 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 fai r in MAP in response to captopril and hexamethonium than the respectiv e control group with intact baroreceptors suggesting an overactivity o f both systems after SAD in normotensive, renal hypertensive and spont aneously 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.