Studies on the role of intracellular sodium and calcium in the central regulation of arterial pressure.
Cerebroventricular infusions of hyperosmotic Na+ solutions, ouabain, and/or angiotensin II (A-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 centrally mediated pressor effects of hyperosmotic Na+ and A-II. Hence, the data suggested that the magnitude of the central pressor effects of A-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 is essential for triggering these central effects. These studies collectively indicated that disturbances in the Na+-transport in the neuronal cells may account for the involvement of central nervous system in various types of hypertension.
D000804:Angiotensin II / Q000494:pharmacology; D000818:Animals; D001794:Blood Pressure / Q000187:drug effects; D002118:Calcium / Q000378:metabolism / Q000502:physiology*; D002490:Central Nervous System / Q000187:drug effects / Q000502:physiology*; D004285:Dogs; D015736:Felodipine; D009543:Nifedipine / Q000031:analogs & derivatives / Q000494:pharmacology; D010042:Ouabain / Q000494:pharmacology; D012964:Sodium / Q000378:metabolism / Q000502:physiology*
D000804:Angiotensin II; D010042:Ouabain; D012964:Sodium; D009543:Nifedipine; D015736:Felodipine; D002118:Calcium