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.
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(-6) M) 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 hyperosmotic 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.
D000804:Angiotensin II / Q000008:administration & dosage / Q000494:pharmacology*; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects*; D001921:Brain / Q000187:drug effects; D002118:Calcium / Q000502:physiology*; D004285:Dogs; D015736:Felodipine; D007276:Injections, Intraventricular; D007424:Intracellular Fluid / Q000502:physiology; D008954:Models, Biological; D009543:Nifedipine / Q000031:analogs & derivatives / Q000494:pharmacology; D010042:Ouabain / Q000008:administration & dosage / Q000494:pharmacology*; D012462:Saline Solution, Hypertonic; D012964:Sodium / Q000134:cerebrospinal fluid / Q000502:physiology*; D014628:Vagotomy
D012462:Saline Solution, Hypertonic; D000804:Angiotensin II; D010042:Ouabain; D012964:Sodium; D009543:Nifedipine; D015736:Felodipine; D002118:Calcium