Role of nitric oxide in regulation of retinal blood flow during hypercapnia in cats.

Abstract

To investigate whether nitric oxide (NO) contributes to the regulation of retinal circulation during hypercapnia in cats. NG-nitro-L-arginine-methylester (L-NAME; n=8), a NOS inhibitor; NG-nitro-D-arginine-methylester (D-NAME; n=6), the inactive isomer; or phosphate-buffered saline (PBS; n=8) was injected intravitreously into the cat's eye. A selective neuronal nitric oxide synthase (nNOS) inhibitor, 7-nitroindazole (7-NI; n=6), was injected intraperitoneally. Hypercapnia was induced for 10 minutes by inhalation of 5% carbon dioxide with 21% oxygen and 74% nitrogen. The vessel diameter and blood velocity were measured simultaneously in large retinal arterioles in cats by laser Doppler velocimetry and the retinal blood flow (RBF) calculated. Retinal vascular resistance (RVR) was also estimated. In the PBS group, the vessel diameter (9.5% +/- 2.7%, P<0.05), blood velocity (15.6% +/- 4.4%, P<0.05), and RBF (37.2% +/- 3.7%, P<0.05) increased, and the RVR decreased (-26.0% +/- 2.7%, P<0.05) during hypercapnia. In the L-NAME group, those changes were greatly suppressed in response to hypercapnia. D-NAME was inactive with regard to RBF during hypercapnia. The RBF responses to hypercapnia after the 7-NI injection were significantly attenuated compared with those before 7-NI injection (P<0.05). These results indicate that NO contributes to the increase in RBF during hypercapnia. Furthermore, the NO synthesized by the action of nNOS may participate in regulation of RBF during hypercapnia.