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The 'body fluid pressure control system' relies on the Renin-Angiotensin-aldosterone system: balance studies in freely moving dogs.

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(Na)V) and MABP reveal no correlation. Spontaneous MABP changes do not affect U(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(2) = 0.79). This correlation is even closer when concomitant changes in total body potassium are also considered (r(2) = 0.91). 5. With normal or elevated TBW, long-term MABP changes correlate well with TBW changes (r(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(Na)V is unimpeded. Within this range, pressure-dependent changes in the RAAS mediate the effects of changes in RPP on U(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.

Animals↗
PubMed1993

Evidence for altered transcapillary fluid balance in women with the premenstrual syndrome.

Redistribution of body fluids has been suggested as a possible pathophysiological mechanism for the premenstrual syndrome (PMS). To elucidate this hypothesis, transcapillary fluid balance was studied in ten women with well defined PMS. Wick-methods were used for measuring colloid osmotic and hydrostatic interstitial pressures on the thorax and on the leg. The capillary filtration coefficient was measured by strain gauge plethysmography. From the follicular to the luteal phase the interstitial colloid osmotic pressure on the leg was significantly reduced (mean 3.6 mm Hg, p = 0.005), whereas the interstitial colloid osmotic pressure on the thorax remained constant. The capillary filtration coefficient increased 30% (mean 5.3 x 10(-4) ml/min/100 gm/mm Hg, p = 0.04) from the follicular to the luteal phase. No change was observed in body weight. These findings indicate an instability of vascular regulation in women with premenstrual syndrome, and lend support to the hypothesis that redistribution of fluid, rather than water retention, is responsible for the subjective symptoms such as bloatedness, in the premenstrual syndrome.

Adult↗