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UBC Theses and Dissertations
A technique for the study of factors influencing sodium excretion in the rabbit and its use in examining the role of cephalic sodium concentration in the control of renal sodium excretion Barker, Kimberly Lynn
The regulation of overall body fluid balance as well as fluid sodium concentration and osmolality involves a complex and interrelated sequence of similar receptor and effector mechanisms. In a recent study in conscious dogs, intracarotid infusions of hypertonic saline were performed concurrent with a jugular vein infusion of water at a rate such that only the areas of the brain supplied by the carotid arteries experienced an increase in plasma sodium concentration (Enimeluth et al., 1992). The results of these infusions were then compared to the effects of an identical salt and water load infused as isotonic saline at the same rate into the carotid arteries and jugular vein. It was concluded from these studies that a mechanism regulating sodium excretion in the distribution of the carotid arteries exists in the conscious dog, that the efferent pathway of this mechanism likely involves the release of urodilatin (a natriuretic peptide), and that this occurs in response to changes in osmolality smaller than those required to stimulate the release of vasopressin. In order to further examine these conclusions, we used similar intracarotid infusions of hypertonic and isotonic saline in an anaesthetized rabbit preparation. The preparation used in these experiments was developed so that renal perfusion pressure could be controlled without interrupting renal blood flow at any time during the surgical procedure. This preparation was examined with respect to the state of hydration of the animals, renal function and renal nerve function,, all of which were determined to be normal. Results of experiments done using this preparation do not support the concept of a specific mechanism regulating sodium excretion in the distribution of the carotid arteries that acts independently of renal perfusion pressure. The intracarotid infusion of hypertonic saline did not cause a greater increase in sodium excretion or a greater decrease in renal vascular resistance than the intracarotid infusion of isotonic saline. Immunoreactive atrial natriuretic peptides do not appear to play a role in mediating sodium excretion in this study and, the release of vasopressin and an increase in sodium excretion appeared to occur in response to the same degree of osmotic change.
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