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[Membrane potential depolarization in the porcine ciliary epithelium evoked by nitric oxide]
J C Fleischhauer1, J Flammer, I O Haefliger
1Laboratory for Ocular Pharmacology und Physiology, University Eye Clinic, Basel, Schweiz.
Background:
The present work studies if in porcine ciliary body epithelium the intracellular signal transduction pathway nitric oxide (NO)--guanylate cyclase (GC)--3',5'-cyclic guanosinemonophosphate (cGMP) can change the membrane potential of the epithelium of the ciliary body.
Material And Methods:
Recordings of membrane potentials were done by means of intracellular microelectrodes in the presence of the NO donor Sodium Nitroprusside (SNP; 100 microM; n = 5) or the membrane permeable cGMP analogue 8-parachlorophenyl-thioguanosine-3',5' cyclic monophosphate (8-pCPT-cGMP; 100 microM; n = 5). To test whether the GC is involved in this process, recordings were repeated in both groups in presence or in absence of the GC inhibitor 1-H-(1,2,4)oxadiazole-(4,3-a)quinoxalin-1-one (ODQ; 10 microM; n = 4).
Results:
SNP and 8-pCPT-cGMP both induced significant membrane potential depolarizations (7.7 +/- 1.8 mV and 13.1 +/- 1.3 mV, mean +/- SEM). Membrane depolarizations induced by SNP were significantly inhibited by ODQ (p < 0.01), whereas depolarizations induced by 8-pCPT-cGMP were not altered by the presence of ODQ (p > 0.2).
Conclusions:
Nitric oxide induces depolarizations of the membrane potential in the isolated porcine ciliary body. This process is transduced by activation of the GC. We conclude that nitric oxide might be involved in the regulation of permeability of the cellular membrane for ions in the ciliary body.