Actions for THE ROLE OF SODIUM AND ANGIOTENSIN IN THE REGULATION OF BODY FLUIDS
THE ROLE OF SODIUM AND ANGIOTENSIN IN THE REGULATION OF BODY FLUIDS
- Author
- KAPSHA, JOAN MARIE
- Physical Description
- 151 pages
- Additional Creators
- Pennsylvania State University
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- Summary
- The role of sodium and angiotensin in the regulation of body fluids involves the interaction of brain and peripheral organ systems. Three studies are described. The focus is on hydrational events occurring after manipulation of the brain and peripheral renin-angiotensin system or after alteration of sodium concentration in blood and cerebrospinal fluid (CSF).
In study #1, a new method involving the adaptation of a sodium selective electrode has been devised to measure lateral ventricular CSF sodium concentration in conscious rabbits before and after osmotic and hypovolemic stimuli. The measurements are direct and continuous. This method is used to test the Osmoreceptor and Sodium Receptor Theories for the response to relative cellular dehydrative thirst.
The values obtained by electrode measurement of CSF sodium concentration are the same as those determined in CSF by flame photometry. The correlation coefficient is 0.97. The paired t-test reveals no statistical differences between photometric and electrode measurements of CSF sodium concentration (n = 34). Since the electrodes can be inserted or removed without apparent awareness or discomfort to the rabbit, stable readings can be made indefinitely with periodic recalibration of the electrodes.
Results from measurements of lateral ventricular CSF sodium concentration with a sodium selective electrode during altered hydration states indicate that temporal and directional changes in CSF sodium concentration parallel changes in plasma sodium concentration. Plasma sodium concentration and osmolality increase after 48 hours of water deprivation (48 WD) and after the induction of relative cellular dehydration (RCD) by the iv injection of 2 M NaCl. The CSF sodium concentration of rabbits increases by 10.8 mEq/1 after 48 WD and 7.6 mEq/1 after iv injection of sodium. The CSF sodium concentration increases immediately after injection with 2 M NaCl and rapidly returns to control levels after water gavage. This rapid change suggests an osmotic movement of water into and out of the CSF compartment. If RCD is induced by iv injection of 2 M sucrose, CSF and plasma sodium concentration remain the same as controls. Serum osmolality increases and the rabbits drink water. A rapid osmotic diuresis occurs. If a hypovolemic stimulus (15 ml/kg of 20% polyethylene glycol, sc) is used to induce drinking behavior, no effective biological change occurs in CSF or plasma sodium concentration. No change in plasma or CSF sodium concentration occurs in rabbits injected with isotonic saline (15 ml/kg, sc). The data support an osmoreceptor mechanism for the development of RCD.
The relationship between brain and peripheral actions of angiotensin is investigated in study #2. One difference between brain and peripheral administration of angiotensin is that the former causes natriuresis, whereas the latter conserves sodium. After 10 days, conscious rats maintained on low, normal and high Na('+) diets are injected intraventricularly with 100 ng of angiotensin II. The results show an elevation in plasma vasopressin content in all dietary groups at 1 and 5 minutes, suppression of plasma renin activity in rats on the normal and low Na('+) diets, and the same intake of water in all dietary groups. These responses are beneficial under conditions of Na('+) excess but detrimental in Na('+) deficiency.
In study #3, the choroid plexi are studied as a possible site for the regulation of angiotensin levels in CSF. Angiotensinase and converting enzyme inhibitors are used to optimize in vitro recovery procedures. Renin activity in rat choroid plexi does not change after 48 WD or hypovolemia. Therefore, it is tentatively concluded that choroidal tissue does not regulate CSF angiotensin by altering endogenous renin activity. - Other Subject(s)
- Dissertation Note
- Ph.D. The Pennsylvania State University 1980.
- Note
- Source: Dissertation Abstracts International, Volume: 41-05, Section: B, page: 1734.
- Part Of
- Dissertation Abstracts International
41-05B
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