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S.E. Ohia, E.M. Monjok, K.K. Kaustubh, K.H. Shivers, C.A. Opere; Effect of Hydogen Sulfide on Sympathetic Neurotransmission in the Isolated Porcine Iris–Ciliary Body . Invest. Ophthalmol. Vis. Sci. 2005;46(13):3683.
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The presence of relatively high concentrations of hydrogen sulfide (H2S) in the brain has been linked to some diseases such as Downs Syndrome (Kamoun et al., Am. J. Med. Gen. 116A:310, 2003). It was, therefore, of interest to study the action of this gas on sympathetic neurotransmission in the anterior uvea. Purpose: To investigate pharmacological actions of H2S (using sodium hydrosulfide, NaHS and sodium sulfide, Na2S as H2S donors) on field–stimulated [3H]–norepinephrine ([3H]NE) release from isolated superfused porcine iris–ciliary bodies (ICB). Methods: Isolated porcine ICBs were incubated for 60 min. at 37oC in carbogen–gassed Krebs buffer containing 2.5 µCi/ml [3H]NE. Release of [3H]NE was elicited by 300 d.c. electrical pulses (5 Hz, 2 msec p.d., 60 s, supramaximal voltage). Fractions of the superfusate were collected at 4–minute intervals and analyzed for radioactivity by liquid scintillation spectrometry. All tissues received two stimulations (S1 and S2) 30 min. apart and NaHS or Na2S was added 8 min. before and during the S2 stimulation period. Results: Application of NaHS (0.1–10 µM) and Na2S (1–100 µM) caused a concentration–dependent inhibition of electrically–evoked [3H]NE overflow without affection basal tritium efflux. For instance, an equimolar concentration (1 µM) of NaHS and Na2S inhibited electrically–evoked [3H]NE release by 30% and 20%, respectively. Both propargylglycine (1 mM; inhibitor of cystathionine ß–synthase) and aminooxyacetic acid (1 mM; inhibitor of cystathionine γ–lyase) blocked the inhibitory response elicited by NaHS on evoked [3H]NE release. Conclusions: Both NaHS and Na2S can inhibit the release of electrically–evoked [3H]NE from porcine iris–ciliary bodies, an effect that is dependent on the production of H2S in this tissue. The mechanism that underlies the observed inhibitory effect of H2S on sympathetic neurotransmission is unknown and merits further investigation.
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