BUFFERING OF BLOOD-PRESSURE VARIABILITY BY THE RENIN-ANGIOTENSIN SYSTEM IN THE CONSCIOUS DOG

1. The renin-angiotensin system (RAS) participates in the compensation of major blood pressure disturbances such as haemorrhage and is invol ved in the tonic long-term (> 1. day) maintenance of mean arterial blo od pressure (MABP). Since its contribution to the short-term (< 1 h) b uffering of normal blood pressure variability is not known, this was i nvestigated in resting conscious dogs. 2. The regulatory efficiency an d the response time of the RAS were studied by an acute step reduction of renal artery pressure to 70 mmHg for 1 h using a suprarenal aortic cuff. After a delay of at least 100 s, MABP rose exponentially by 22 +/- 5 mmHg in normal dogs (n = 4), by 6 +/- 3 mmHg after angiotensin c onverting enzyme (ACE) inhibition (n = 4), and by 25 +/- 5 mmHg after ganglionic blockade (n = 4). MABP returned to control after release of the cuff with similar time courses. The time constants of the MABP re sponses were in the range of 20 min. Thus, possible feedback oscillati ons of the RAS would be expected around 0.0025 Hz (1/(4 x 100 s)); a b uffering effect would be possible below this frequency 3. Blood pressu re variability was investigated by spectral analysis of MABP from 3.75 h recordings in the frequency ranges of 0.002-0.003 Hz (feedback osci llations) and below 0.002 Hz (buffering effect). 4. ACE inhibition (n = 7) decreased MABP by 11 +/- 2 mmHg (P < 0.05), but in both frequency ranges integrated spectral density was not affected. ACE inhibition a lso failed to significantly change spectral density in either of the t wo frequency ranges under the following conditions: (1) during ganglio nic blockade (n = 7), (2) during a low-sodium diet (except for a very slight elevation below 0.002 Hz) (n = 7), and (3) when the fall of MAB P induced by ACE inhibition was compensated by an angiotensin II infus ion (11 = 7). 5. It is concluded that in spite of its high regulatory efficiency with an adequate response time the RAS does not directly co ntribute to the short-term buffering of blood pressure variability, no r does it give rise to feedback oscillations under normal resting cond itions. Even if the RAS is stimulated by sodium restriction its contri bution to short-term blood pressure buffering is only marginal.