Title : NADPH oxidase and PKC contribute to increased Na transport by the thick ascending limb during type 1 diabetes.

Pub. Date : 2012 Feb

PMID : 22203737






2 Functional Relationships(s)
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1 The PKC inhibitor calphostin C (1 mumol/L) or the PKCalpha/beta inhibitor Go6976 (1 mumol/L) decreased furosemide-sensitive O(2) consumption in both groups, achieving values that did not differ between sham and diabetic. Superoxides protein kinase C, alpha Rattus norvegicus
2 We conclude that NADPH oxidase and PKC (primarily PKCalpha) contribute to an increase in O(2) consumption by the mTAL during type 1 diabetes through effects on the ouabain-sensitive Na(+)-K(+)-ATPase and furosemide-sensitive Na(+)-K(+)-2Cl(-) cotransporter that are primarily responsible for active transport Na(+) reabsorption by this nephron segment. Superoxides protein kinase C, alpha Rattus norvegicus