TY - JOUR
T1 - Effects of inhibition of neuronal nitric oxide synthase on basal retinal blood flow regulation
AU - Tummala, Shanti R.
AU - Benac, Sanja
AU - Tran, Harry
AU - Vankawala, Anand
AU - Zayas-Santiago, Astrid
AU - Appel, Alyssa
AU - Kang Derwent, Jennifer J.
PY - 2009/11
Y1 - 2009/11
N2 - Nitric oxide (NO) has been observed to regulate blood flow under basal and stimulated conditions in the retina. Recent evidence suggests that NO produced by neuronal nitric oxide synthase (nNOS) may regulate blood flow in addition to that produced by endothelial nitric oxide synthase (eNOS). The objective of the current study was to investigate the contribution of NO produced by nNOS in the regulation of basal retinal blood flow. A non-specific NOS inhibitor N (G)-nitro-l-arginine methyl ester (l-NAME) and the specific nNOS inhibitors 1-(2-trifluoromethylphenyl) imidazole (TRIM) and (4S)-N-(4-amino-5 [aminoethyl] aminopentyl)-N-nitroguanidine (AAAN) were injected into the vitreous (intravitreal) of Long-Evans rats. Vessel diameters, velocities and volumetric blood flow rates (VBF) in the retinal circulation were determined prior to and in 30-min intervals for 4-4.5 h after injection. In addition, the basal amount of nNOS in the rat retina was quantified using a specific enzyme linked immunoassay (ELISA). Treatment with l-NAME and TRIM significantly decreased diameters and VBF. Compared with saline, treatment with l-NAME and TRIM produced a significant (p < 0.001) decrease of ∼12-17% in vessel diameters. Treatment with AAAN significantly decreased vessel diameters and venous VBF. Compared with saline AAAN produced a significant decrease of ∼7% in arterial (p < 0.001) and 5% in venous (p = 0.011) diameters, respectively. The amount of nNOS in the rat retina was 0.17 ± 0.0147 pmol mg-1 of dry retina. The results suggest that though inhibition of nNOS decreases basal diameters, constant VBF is maintained in the retinal circulation.
AB - Nitric oxide (NO) has been observed to regulate blood flow under basal and stimulated conditions in the retina. Recent evidence suggests that NO produced by neuronal nitric oxide synthase (nNOS) may regulate blood flow in addition to that produced by endothelial nitric oxide synthase (eNOS). The objective of the current study was to investigate the contribution of NO produced by nNOS in the regulation of basal retinal blood flow. A non-specific NOS inhibitor N (G)-nitro-l-arginine methyl ester (l-NAME) and the specific nNOS inhibitors 1-(2-trifluoromethylphenyl) imidazole (TRIM) and (4S)-N-(4-amino-5 [aminoethyl] aminopentyl)-N-nitroguanidine (AAAN) were injected into the vitreous (intravitreal) of Long-Evans rats. Vessel diameters, velocities and volumetric blood flow rates (VBF) in the retinal circulation were determined prior to and in 30-min intervals for 4-4.5 h after injection. In addition, the basal amount of nNOS in the rat retina was quantified using a specific enzyme linked immunoassay (ELISA). Treatment with l-NAME and TRIM significantly decreased diameters and VBF. Compared with saline, treatment with l-NAME and TRIM produced a significant (p < 0.001) decrease of ∼12-17% in vessel diameters. Treatment with AAAN significantly decreased vessel diameters and venous VBF. Compared with saline AAAN produced a significant decrease of ∼7% in arterial (p < 0.001) and 5% in venous (p = 0.011) diameters, respectively. The amount of nNOS in the rat retina was 0.17 ± 0.0147 pmol mg-1 of dry retina. The results suggest that though inhibition of nNOS decreases basal diameters, constant VBF is maintained in the retinal circulation.
KW - basal retinal blood flow
KW - neuronal nitric oxide synthase
KW - nitric oxide
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U2 - 10.1016/j.exer.2009.07.014
DO - 10.1016/j.exer.2009.07.014
M3 - Article
C2 - 19646435
AN - SCOPUS:70349440845
SN - 0014-4835
VL - 89
SP - 801
EP - 809
JO - Experimental Eye Research
JF - Experimental Eye Research
IS - 5
ER -