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Johannes C. Fleischhauer, Jean-Louis Bény, Josef Flammer, Ivan O. Haefliger; NO/cGMP Pathway Activation and Membrane Potential Depolarization in Pig Ciliary Epithelium. Invest. Ophthalmol. Vis. Sci. 2000;41(7):1759-1763.
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© ARVO (1962-2015); The Authors (2016-present)
purpose. To investigate whether in isolated porcine ciliary processes,
stimulation of the nitric oxide (NO)-guanylate cyclase
(GC)-3′,5′-cyclic guanosine monophosphate (cGMP) pathway modulates
ciliary epithelial transmembrane potential.
methods. Changes in transmembrane potential induced by the two NO donors, sodium
nitroprusside (SNP; 100 μM) and S-nitroso-N-acetyl-penicillamine
(SNAP; 100 μM), or by the cGMP-analogue
monophosphate (8-pCPT-cGMP; 100 μM) were measured with
microelectrodes in the presence or in the absence of the GC-inhibitor
1-H-(1,2,4)oxadiazole(4,3-α)quinoxalin-1-1 (ODQ; 10 μM). The effect
of 8-pCPT-cGMP was also assessed in the presence of the anion channel
inhibitors niflumic acid (100 μM), diisothiocyanatostilbene-2,2′
disulfonic acid (DIDS; 1 mM), anthracene-9-carboxylic acid (9-AC; 1
mM), or the K+ channel blocker tetraethylammonium
chloride (TEA; 10 mM). cGMP production was measured by immunoassay.
results. Significant membrane depolarizations (P < 0.05–0.001; n = 5−8) were induced by SNP (6 ± 1 mV;
mean ± SEM), SNAP (8 ± 1 mV), or 8-pCPT-cGMP (13 ± 1
mV). In presence of ODQ, the effect of SNP and SNAP were significantly
inhibited (−2 ± 0 mV and 0 ± 0 mV, respectively; P < 0.05; n = 5−6), but not
depolarizations elicited by 8-pCPT-cGMP. These were prevented
(P < 0.05–0.01; n = 5) by niflumic
acid (1 ± 1 mV), DIDS (1 ± 1 mV), or 9-AC (5 ± 1 mV),
but not by TEA (12 ± 2 mV). The increase in cGMP production
induced by SNP (9.5-fold) was inhibited by ODQ (P <
0.001; n = 6).
conclusions. Activation of the NO-GC-cGMP pathway modulates epithelial transmembrane
potential in isolated porcine ciliary
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