1987
DOI: 10.1016/0006-8993(87)90326-x
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Active sodium-potassium transports in skeletal muscles of deoxycorticosterone hypertensive rats

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1987
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Cited by 8 publications
(3 citation statements)
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“…Because of similar findings in aortas and skeletal muscle of hypertensive rats treated with DOC-salt (Figs. 1A and 2), the up regulation of al-and 13-subunit mRNA expression is clearly not pressure-related, but could be secondary to alterations in Na+ flux induced by DOC-salt treatment; other studies have documented increased Na+ influx in these tissues (17,18). The increase in a1 mRNA correlates with increased vascular Na+,K+-ATPase activity in hypertensive rats treated with DOC-salt (19,20).…”
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confidence: 90%
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“…Because of similar findings in aortas and skeletal muscle of hypertensive rats treated with DOC-salt (Figs. 1A and 2), the up regulation of al-and 13-subunit mRNA expression is clearly not pressure-related, but could be secondary to alterations in Na+ flux induced by DOC-salt treatment; other studies have documented increased Na+ influx in these tissues (17,18). The increase in a1 mRNA correlates with increased vascular Na+,K+-ATPase activity in hypertensive rats treated with DOC-salt (19,20).…”
mentioning
confidence: 90%
“…To further test the possibility that the ABPP is an HSPG core protein, we reacted growth-conditioned medium from a variant (F3) of PCl2 that contains no cell-surface HSPG (18) with the antibody to ABPP before and after heparinase 2 digestion. Although there was detectable ABPP antigen secreted by the F3 PCl2 variant (Fig.…”
mentioning
confidence: 99%
“…In contrast with the stimulation of enzyme activity promoted by aldosterone or DEX, the mineralocorticoid deoxycorticosterone ace- tate given in pharmacological amounts inhibited enzyme activity and 8 1 -subunit expression in specific brain areas (Grillo et al ., 1989(Grillo et al ., , 1991 and in erythrocyte membranes (Chen and Lin-Shiau, 1988) . Also, in deoxycorticosterone acetate-treated hypertensive rats, there was a marked K + loss and Na' accumulation in muscle, suggesting Na + ,K + -ATPase inhibition (Nagaoka et al, 1987) . Therefore, it is still unclear whether a single receptor or both type I and type 11 receptors become occupied in the CNS during changes of Na + ,K + -ATPase biosynthesis due to treatment with adrenal hormones possessing glucocorticoid or mineralocorticoid activity.…”
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confidence: 92%