Neural, Hormonal and Renal Interactions in Long-Term Blood Pressure Control: THE 'BODY FLUID PRESSURE CONTROL SYSTEM' RELIES ON THE RENIN-ANGIOTENSIN-ALDOSTERONE SYSTEM: BALANCE STUDIES IN FREELY MOVING DOGS

• Published in: Clinical and experimental pharmacology & physiology 2005-05, Vol.32 (5-6), p.394-399
• Main Authors: Seeliger, Erdmann, Wronski, Thomas, Ladwig, Mechthild, Rebeschke, Till, Persson, Pontus B, Reinhardt, H Wolfgang
• Format: Article
• Language: English
• ISSN: 0305-1870; 1440-1681
• DOI: 10.1111/j.1440-1681.2005.04201.x

1. The physiological role of the 'renal body fluid pressure control system', including the intrarenal mechanism of 'pressure natriuresis', is uncertain. 2. Balance studies in freely moving dogs address the following questions: (i) what is the physiological contribution of pressure natriuresis to the control of total body sodium (TBS); (ii) to what extent is long-term mean arterial blood pressure (MABP) determined by TBS and total body water (TBW); and (iii) during Na accumulation, is Na stored in an osmotically inactive form? 3. Diurnal time-courses of Na excretion (U sub(Na)V) and MABP reveal no correlation. Spontaneous MABP changes do not affect U sub(Na)V. The long-term 20% reduction of renal perfusion pressure (RPP) results in Na retention via pressure-dependent stimulation of the renin-angiotensin-aldosterone system (RAAS), not via a pressure natriuresis mechanism. Prevention of pressure natriuresis does not result in ongoing Na retention when the RAAS is operative. The long-term 20% elevation of RPP induced by sustained TBS elevation facilitates Na excretion via pressure natriuresis, but does not restore TBS to normal. 4. Changes in TBW correlate well with changes in TBS (r super(2) = 0.79). This correlation is even closer when concomitant changes in total body potassium are also considered (r super(2) = 0.91). 5. With normal or elevated TBW, long-term MABP changes correlate well with TBW changes (r super(2) = 0.69). At lowered TBW, no correlation is found. 6. In conclusion, the physiological role of pressure natriuresis is limited. Pressure natriuresis does not appear to be operative when RPP is changed from -20 to +10% and neurohumoral control of U sub(Na)V is unimpeded. Within this range, pressure-dependent changes in the RAAS mediate the effects of changes in RPP on U sub(Na)V. Pressure natriuresis may constitute a compensating mechanism under pathophysiological conditions of substantial elevation of RPP. A large portion of the long-term changes in MABP are attributable to changes in TBW. The notion of osmotically inactive Na storage during Na accumulation appears to be invalid.