The isolated human retinal arterioles (
n = 17) developed stable basal tone (i.e., constricted to 69% ± 1% of their maximum diameter) at 36°C to 37°C bath temperature with 55 cm H
2O intraluminal pressure. The average resting and maximum diameters of the vessels were 43 ± 2 μm (range, 32–64 μm) and 63 ± 3 μm (range, 50–89 μm), respectively. In the pig study, the average resting and maximum diameters were 52 ± 2 μm and 85 ± 2 μm (
n = 26), respectively. Both human (
Fig. 2A) and porcine (
Fig. 2B) retinal arterioles dilated to bradykinin in a dose-dependent manner with threshold responses at 1 pM and 10 pM, respectively. Bradykinin exhibited comparable potency (human EC
50 = 0.15 nM; porcine EC
50 = 0.50 nM;
P = 0.06) and elicited nearly 90% maximum dilation at 10 nM in both vessel types (
Fig. 2). Subsequent administration of L-NAME abolished these vasodilator responses, except at the last concentration (10 nM), where nearly 20% dilation remained (
Fig. 2). Adenosine also caused dose-dependent dilation of human (
Fig. 3A) and porcine (
Fig. 3B) retinal arterioles, with 80% to 90% maximum dilation at 0.1 mM. However, adenosine exhibited greater potency (human EC
50 = 0.26 μM; porcine EC
50 = 3.6 μM;
P < 0.05) in human vessels. Exposure to L-NAME consistently reduced the dilation of human vessels to adenosine in a significant manner (
Fig. 3), whereas the response of porcine vessels was significantly reduced at 1 μM and 10 μM adenosine.
Figure 4 displays graded vasodilation of both human and porcine retinal arterioles when the pressure gradient, and thus luminal flow, was increased in a stepwise manner. Under control conditions, the highest flow elicited nearly 50% to 60% of maximum dilation in retinal arterioles from both species; but in the presence of L-NAME, the responses were abolished (zero flow vs. all steps of flow; one-way ANOVA,
P > 0.05). Furthermore, both human (
Fig. 5A) and porcine (
Fig. 5B) retinal arterioles dilated dose dependently to the endothelium-independent NO donor sodium nitroprusside with threshold response at 10 nM, comparable potency (human EC
50 = 0.42 μM; porcine EC
50 = 0.87 nM;
P = 0.10) and maximum dilation of approximately 75% to 80% at 10 μM. L-NAME did not alter this vasodilator response (
Fig. 5).