Carbachol and nitric oxide inhibition of Na,K-ATPase activity in bovine ciliary processes.

摘要: Purpose Nitric oxide (NO) donors and cholinergic agents decrease intraocular pressure, in part because they induce a aqueous humor production. Because Na,K-adenosine triphosphatase (ATPase) is involved formation, this study was conducted to investigate the hypothesis that NO cholinomimetics regulate its activity bovine ciliary processes. Methods Bovine tissue slices were incubated with agonists antagonists physiological buffer vitro. Na,K-ATPase determined by assaying hydrolysis of adenosine triphosphate (ATP) suspended permeabilized slices. Results Carbachol-induced inhibition correlated increases cGMP. This abolished muscarinic blocker atropine, inhibitor N(w)-nitro-L-arginine (L-NAME) soluble guanylate cyclase 1H-[1,2,4]oxadiazolo[4,3-a]quinoxalin-1-one (ODQ). Sodium nitroprusside (SNP) mimicked actions carbachol. The SNP-induced an increase cGMP also ODQ. Both 8-bromo (Br)-cGMP okadaic acid inhibited activity. Conclusions involves receptor activation. That SNP mimics L-NAME reverses carbachol's effect on suggests carbachol are mediated NO. Carbachol's SNP's effects Inhibition 8-Br-cGMP indicates protein phosphorylation events may mediate