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Dorette Z. Ellis, James A. Nathanson, Jason Rabe, Kathleen J. Sweadner; Carbachol and Nitric Oxide Inhibition of Na,K-ATPase Activity in Bovine Ciliary Processes. Invest. Ophthalmol. Vis. Sci. 2001;42(11):2625-2631. doi: https://doi.org/.
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purpose. Nitric oxide (NO) donors and cholinergic agents decrease intraocular
pressure, in part because they induce a decrease in aqueous humor
production. Because Na,K-adenosine triphosphatase (ATPase) is involved
in aqueous humor formation, this study was conducted to investigate the
hypothesis that NO and cholinomimetics regulate its activity in bovine
methods. Bovine tissue slices were incubated with agonists and antagonists in a
physiological buffer in vitro. Na,K-ATPase activity was determined by
assaying hydrolysis of adenosine triphosphate (ATP) in suspended
permeabilized tissue slices.
results. Carbachol-induced inhibition of Na,K-ATPase activity correlated with
increases in cGMP. This inhibition was abolished by the muscarinic
blocker atropine, the NO inhibitor N w-nitro-l-arginine
(l-NAME) and the soluble guanylate cyclase inhibitor
1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). Sodium
nitroprusside (SNP) mimicked the actions of carbachol. The SNP-induced
decrease in Na,K-ATPase activity correlated with an increase in cGMP
and was also abolished by ODQ. Both 8-bromo (Br)-cGMP and okadaic acid
also inhibited Na,K-ATPase activity.
conclusions. Carbachol-induced inhibition of Na,K-ATPase activity involves
muscarinic receptor activation. That SNP mimics and l-NAME
reverses carbachol’s effect on Na,K-ATPase activity suggests that the
actions of carbachol are mediated by NO. Carbachol’s and SNP’s
effects on Na,K-ATPase activity involved soluble guanylate cyclase and
cGMP. Inhibition of Na,K-ATPase activity by 8-Br-cGMP and okadaic acid
indicates that protein phosphorylation events may mediate SNP-induced
inhibition of Na,K-ATPase activity.
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