Title : Interaction between nitric oxide and superoxide in the macula densa in aldosterone-induced alterations of tubuloglomerular feedback.

Pub. Date : 2013 Feb 1

PMID : 23220724






4 Functional Relationships(s)
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1 We hypothesize that aldosterone enhances O(2)(-) production in the MD mediated by protein kinase C (PKC), which buffers the effect of NO in control of TGF response. Superoxides protein kinase C, alpha Mus musculus
2 To determine if PKC is involved in aldosterone-induced O(2)(-) production, we exposed the O(2)(-) cells to a nonselective PKC inhibitor chelerythrine chloride, a specific PKCalpha inhibitor Go6976, or a PKCalpha siRNA, and the aldosterone-induced increase in O(2)(-) production was blocked. Superoxides protein kinase C, alpha Mus musculus
3 To determine if PKC is involved in aldosterone-induced O(2)(-) production, we exposed the O(2)(-) cells to a nonselective PKC inhibitor chelerythrine chloride, a specific PKCalpha inhibitor Go6976, or a PKCalpha siRNA, and the aldosterone-induced increase in O(2)(-) production was blocked. Superoxides protein kinase C, alpha Mus musculus
4 These data indicate that aldosterone-stimulated O(2)(-) production in the MD buffers the effect of NO in control of TGF response, an effect that was mediated by PKCalpha. Superoxides protein kinase C, alpha Mus musculus