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Renyi Wu, Ke Yao, Josef Flammer, Ivan O. Haefliger; Role of Anions in Nitric Oxide-Induced Short-Circuit Current Increase in Isolated Porcine Ciliary Processes. Invest. Ophthalmol. Vis. Sci. 2004;45(9):3213-3222. doi: https://doi.org/10.1167/iovs.03-1252.
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purpose. To investigate how nitric oxide (NO) modulates short-circuit current (Isc) in isolated porcine ciliary processes.
methods. Isc changes (Ussing-type chamber) induced either by the NO donors SNP or SIN-1, or by the cGMP analogue 8-pCPT-cGMP were assessed. The effect of inhibitors of guanylate cyclase (10 μM ODQ, 100 μM LY83583), protein kinase G (30 μM Rp-8-pCPT-cGMP, 3 μM KT 5823), protein kinase A (1 μM KT 5720), or protein kinase C (1 μM Go6983) on SNP- or 8-pCPT-cGMP–induced Isc changes were investigated. The effect of inhibitors of anion channel (100 μM niflumic acid, 1 mM DIDS, and 1 mM 9-AC), K+-channel (10 mM TEA, 10 mM BaCl2), Na+-channel blockers (1 mM amiloride), Na+-K+-2Cl− cotransporter inhibitor (0.5 mM bumetanide), or carbonic anhydrase inhibitor (1 mM acetazolamide) was studied. In Cl−- or HCO3 −-free Krebs-Ringer solution, the effect of SNP- or 8-pCPT-cGMP–induced Isc changes was accessed.
results. SNP, SIN-1, or 8-pCPT-cGMP increased Isc with a change in the potential difference that became more negative toward the nonpigmented epithelium (aqueous) side. The Isc increase induced by SNP or SIN-1, but not by 8-pCPT-cGMP, was prevented by ODQ and LY83583. SNP- and 8-pCPT-cGMP–induced Isc increases were prevented by Rp-8-pCPT-cGMP or KT5823 (but not by KT5720 or Go6983), or by niflumic acid, DIDS, 9-AC, or acetazolamide (but not by TEA, BaCl2, amiloride, or bumetanide). The effect of SNP and 8-pCPT-cGMP was abolished in Cl−- and reduced in HCO3 −-free solutions.
conclusions. NO activates a guanylate cyclase-cGMP-protein kinase G pathway that appears to stimulate stroma-to-aqueous anionic transport, possibly Cl−, in porcine ciliary epithelium.
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