Introduction
Whereas total body sodium (TBS) is well known to be a major determinant of long-term mean arterial blood pressure (MABP), when TBS is increased or normal, little is known about this relationship during decreased TBS. With its Na-retaining hormones angiotensin II (A II) and aldosterone (Aldo), the renin-angiotensin-aldosterone system (RAAS) is a prime candidate in control of sodium balance, and thus of TBS. This study aims to determine the role of RAAS for control of sodium balance and MABP following experimentally induced deficit of TBS.
Methods
Balance studies were performed in freely moving dogs, using 3 protocols (P). In all P, TBS was reduced by peritoneal dialysis (PD) by 10 % on day 1. On days 1 and 2, dogs were on low sodium intake, on days 3 and 4 on high sodium intake. In P1, RAAS was not inhibited; in P2, angiotensin converting enzyme inhibition (ACEI) was applied on days 2 to 4; in P3, an aldosterone-antagonist (AA) was additionally applied on these days.
Results
In all P, on days 1 and 2 (low sodium intake), TBS remained on the reduced level gained by PD. In P1, the deficit of TBS is immediately corrected by sodium retention, when sodium is offered with the food (day 3). This is achieved by stimulation of RAAS. However, the deficit is corrected even during ACEI (P2). This is due to stimulation of Aldo release, that is independent from A II, because the deficit is not corrected during AA (P3). By PD, sodium but not water is withdrawn. Yet osmoregulatory mechanisms result in a negative water balance during day 1, thus total body water (TBW) decreases. On days 2 to 4, water balances mirrored sodium balances in all P. MABP barely decreased in P1 despite the deficit in TBS and TBW (days 1 and 2). MABP is maintained by volume-independent mechanisms, in particular, vasoconstrictory action of A II, as shown by P2: when ACEI was started on day 2, MABP decreased by 15 mmHg from day 1 to 2, although TBW remained constant. With ongoing ACEI, MABP became volume-dependent again: whereas MABP rose in parallel with TBS and TBW in P2 (day 3), it remained decreased in P3.
Conclusions
RAAS is a major controller of sodium balance and MABP during reduced TBS. First, the vasoconstrictory action of A II stabilizes MABP in face of an acute deficit of TBS and TBW. Second, stimulation of renin, and thus, A II, and, even independently from A II, of Aldo release, play a pivotal role in restoring TBS, thus maintaining long-term MABP.
References