TY - JOUR
T1 - Cyclic GMP, sodium nitroprusside and sodium azide reduce aqueous humour formation in the isolated arterially perfused pig eye
AU - Shahidullah, Mohammad
AU - Yap, Maurice
AU - To, Chi Ho
PY - 2005/5
Y1 - 2005/5
N2 - The effect of nitric oxide (NO) on aqueous humour formation (AHF) and intraocular pressure (IOP) was studied using NO donors, sodium azide (AZ) and sodium nitroprusside (SNP). Using the porcine arterially perfused eye preparation, drug effects on AHF and IOP were measured by fluorescein dilution and manometry, respectively. Perfusion pressure of the ocular vasculature was also monitored using digital pressure transducer and pen recorder. L-Arginine (1.0 mM), a precursor of NO, but not D-arginine (1.0 mM), the inactive analogue, produced a significant reduction in AHF (28.5%) and IOP (21.1%). L-NAME (L-nitro-L-arginine) (10-100 μM), an NO synthase inhibitor, had no effect on AHF and IOP. However, L-NAME (100 μM) completely reversed L-arginine's effect. AZ and SNP reduced the AHF and IOP dose-dependently. AZ at 100 nM, 1 and 10 μM reduced AHF by 26.0, 39.7 and 51.7% and IOP by 10.8, 17.3 and 24.0%, respectively. SNP at 1, 10 and 100 μM reduced the AHF by 6.0, 24.2 and 35.4% and IOP by 3.5, 9.5 and 15.5%, respectively. 8-pCPT-cGMP (8-para-chlorophenyl- thioguanosine-3′,5′-cyclic guanosine monophosphate, 10 μM), a cGMP analogue, also reduced the AHF (34.9%) and IOP (15.9%). The effects of AZ and SNP on the AHF and IOP were blocked by a soluble guanylate cyclase inhibitor ODQ (10 μM), whereas ODQ alone or combined with 8-pCPT-cGMP had no effect on the AHF and IOP. None of the drugs had any significant effect on ocular vasculature. The reduction of the AHF and IOP in the arterially perfused pig eye by nitrovasodilators is likely to involve the NO-cGMP pathway.
AB - The effect of nitric oxide (NO) on aqueous humour formation (AHF) and intraocular pressure (IOP) was studied using NO donors, sodium azide (AZ) and sodium nitroprusside (SNP). Using the porcine arterially perfused eye preparation, drug effects on AHF and IOP were measured by fluorescein dilution and manometry, respectively. Perfusion pressure of the ocular vasculature was also monitored using digital pressure transducer and pen recorder. L-Arginine (1.0 mM), a precursor of NO, but not D-arginine (1.0 mM), the inactive analogue, produced a significant reduction in AHF (28.5%) and IOP (21.1%). L-NAME (L-nitro-L-arginine) (10-100 μM), an NO synthase inhibitor, had no effect on AHF and IOP. However, L-NAME (100 μM) completely reversed L-arginine's effect. AZ and SNP reduced the AHF and IOP dose-dependently. AZ at 100 nM, 1 and 10 μM reduced AHF by 26.0, 39.7 and 51.7% and IOP by 10.8, 17.3 and 24.0%, respectively. SNP at 1, 10 and 100 μM reduced the AHF by 6.0, 24.2 and 35.4% and IOP by 3.5, 9.5 and 15.5%, respectively. 8-pCPT-cGMP (8-para-chlorophenyl- thioguanosine-3′,5′-cyclic guanosine monophosphate, 10 μM), a cGMP analogue, also reduced the AHF (34.9%) and IOP (15.9%). The effects of AZ and SNP on the AHF and IOP were blocked by a soluble guanylate cyclase inhibitor ODQ (10 μM), whereas ODQ alone or combined with 8-pCPT-cGMP had no effect on the AHF and IOP. None of the drugs had any significant effect on ocular vasculature. The reduction of the AHF and IOP in the arterially perfused pig eye by nitrovasodilators is likely to involve the NO-cGMP pathway.
KW - Aqueous humour formation
KW - Intraocular pressure
KW - NO donors
KW - Pig eye
KW - cGMP
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U2 - 10.1038/sj.bjp.0706156
DO - 10.1038/sj.bjp.0706156
M3 - Article
C2 - 15711584
AN - SCOPUS:18744373015
SN - 0007-1188
VL - 145
SP - 84
EP - 92
JO - British Journal of Pharmacology
JF - British Journal of Pharmacology
IS - 1
ER -