PHYSIOLOGICAL SIGNIFICANCE OF NA+ K+-ATPASE ACTIVITY IN THE CENTRAL-NERVOUS-SYSTEM AND ENDOGENOUS SODIUM-PUMP INHIBITORS IN THE NEURAL REGULATION OF ARTERIAL BLOOD-PRESSURE/

In anesthetized Sprague-Dawley rats, cerebrolateral ventricular admini stration of potassium chloride solutions (KCl, 0.375-1.25 mumol, i.c.v .) produced concentration-dependent reductions in the arterial blood p ressure and heart rate. These responses were significantly attenuated by prior i.c.v.-administration ouabain, a selective inhibitor of the N a+ pump, and by endothelin (ET-1), an endogenous peptide that is prese nt in the CNS, suggesting that this peptide may participate in the neu ral regulation of arterial pressure via modulation of Na+-pump activit y. Although both acute fluid volume expansion and/or osmotic stimulus have been shown to facilitate the release of the endogenous Na+-pump i nhibitor(s) into the circulation, only volume expansion significantly attenuated the cardiovascular effects of i.c.v. potassium chloride. Th ese observations collectively suggest that the Na+,K+-ATPase activity in CNS and Na+-pump inhibitors may play a significant role in the cent ral regulation of arterial pressure under certain physiological condit ions.