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Vanadate at doses from 10(-4.5) to 10(-3) M caused a dose-dependent contraction of the rat aorta in vitro. Aortas of Dahl salt-hypertension sensitive (S) rats responded to vanadate with a greater contraction than Dahl salt-hypertension resistant (R) rats. In contrast, S and R aortic responses to depolarization with potassium were equal, and responses to norepinephrine were less in S than R. The mechanism by which vanadate causes the aortic response was studied in S rats. In aortic smooth muscle sodium-loaded by exposure to low potassium media followed by a norepinephrine-induced contraction, a relaxation induced with 5 mM potassium was not influenced by 10(-3) M vanadate. Since this potassium-induced relaxation is known to be a reflection of (NaK)-ATPase activity, these data show that vanadate (up to 10(-3) M does not inhibit (Na,K)-ATPase in intact smooth muscle cells although it is a known potent inhibitor of (Na,K)-ATPase in isolated cell membrane preparations. Response to vanadate was not changed by alpha-blockade with phentolamine or by blocking (Na,K)-ATPase with ouabain. Vanadate contraction was blocked by 4,4'-diisothiocyano-2,2'-disulfonic acid stilbene, a known inhibitor of anion transport, suggesting that vanadate anions must enter smooth muscle cells to induce contraction.

Aortic responses to vanadate: independence from (Na,K)-ATPase and comparison of Dahl salt-sensitive and salt-resistant rats.