Na+/K+-ATPase regulation in Dahl salt-sensitive and salt-resistant rats.
Circulating Na+/K+-ATPase inhibitors have been implicated in volume-expanded forms of hypertension. Inhibition of vascular smooth muscle cell Na+/K+-ATPase has been demonstrated to elevate intracellular Ca2+ levels and enhance contractility, thus providing a mechanism of raised peripheral resistance. In cells chronically subjected to Na+/K+-ATPase inhibition, however, new Na+/K+-ATPase molecules are synthesized, which then restore the intracellular milieu to preinsult conditions. Restoral of the preinsult intracellular milieu in vascular smooth muscle cells would then be expected to lead to the reduction of muscle cell contractility and peripheral resistance. Thus circulating Na+/K+-ATPase inhibitors may not be effective in eliciting chronic forms of hypertension unless the target cell "homeostatic response" is impaired. We demonstrate an apparent such impairment in Dahl salt-sensitive rats, a genetic model of salt-sensitive hypertension.
Rayson
B M
BM
Department of Physiology, Cornell University Medical College, New York Hospital, New York 10021.
D000818:Animals; D017301:Ca(2+) Mg(2+)-ATPase / Q000378:metabolism; D004039:Diet, Sodium-Restricted; D007679:Kidney Medulla / Q000201:enzymology; D007700:Kinetics; D008297:Male; D010042:Ouabain / Q000494:pharmacology; D011188:Potassium / Q000378:metabolism; D011506:Proteins / Q000032:analysis; D051381:Rats; D011919:Rats, Inbred Strains; D012964:Sodium / Q000378:metabolism; D000254:Sodium-Potassium-Exchanging ATPase / Q000378:metabolism*; D000097795:ATPase Inhibitory Protein
D017301:Ca(2+) Mg(2+)-ATPase; D010042:Ouabain; D011188:Potassium; D011506:Proteins; D012964:Sodium; D000254:Sodium-Potassium-Exchanging ATPase; D000097795:ATPase Inhibitory Protein