Studies on The Role of Intracellular Sodium and Calcium in The Centrally Mediated Pressor Effects of CSF [Na+], Ouabain and Angiotensin II in Anesthetized Dogs

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Abstract
Cerebroventricular infusions of hyperosmotic Na+solutions, ouabain and/or Angiotensin-II produced significant increases in the arterial blood pressure in chloralose anesthetized, vagotomized dogs. A lower concentration of ouabain (10−6M) which did not alter blood pressure, significantly potentiated the centrally mediated pressor effects of hyperosmotic Na+and angiotensin-II. Hence, the data suggested that the magnitude of the central pressor effects of Angiotensin-II or hyperosmotic Na+may depend upon net accumulation of sodium in the neuronal cells. Prior cerebroventricular infusions of felodipine, a “calcium antagonist,” significantly inhibited the pressor actions of higher concentrations of ouabain as well as that of hyperosomotic Na+- solutions, indicating that cellular calcium may be essential for triggering these central effects. These studies collectively indicate that disturbances in the Na+-transport in the neuronal cells may account for the involvement of the central nervous system in various types of hypertension.