[The vasodilation mechanisms of human erythrocyte-derived depressing factor]

To evaluate the effect of EDDF a new erythrocyte-derived depressing factor, on the NO/cGMP pathway in aorta of normal rats and rat, with hypertension induced by L-NNA.

Thirty male Wistar rats aged 10 weeks were divided into two groups: L-NNA group and control group, 15 rats for each group. L-N(G)-nitro-arginine (L-NNA) was injected into the abdominal cavity of the rats in the L-NNA group at dose of 15 mg/kg twice a day for four weeks. Normal saline was injected the same way in the control group. The levels of cGMP in aorta and plasma were measured by radioimmunoassay and (3)H-L-arg incorporation. NOS was measured by immunohistochemistry.

One day after injection of L-arg, the blood pressure of the experimental rats began to rise remarkably (18.8 kPa vs 16.4 kPa, P < 0.05), and then remained at a high level. The L-arg. transfer rate (pmol small middle dotmg(-1) small middle dotpr small middle dotmin(-1)) of aorta in L-NNA group was significantly lower than that of control group (13.0 +/- 0.9 vs 16.8 +/- 1.2 P < 0.05). After incubation with EDDF (10(-4) g/ml), the L-arg transfer rate and cGMP level of aorta were remarkably increased in normal rats (20.1 +/- 0.9 vs 16.8 +/- 1.2, P < 0.05 and 233 +/- 14 vs 187 +/- 10, P < 0.05). The L-arg transfer rate and cGMP level of aorta remained unchanged afeter incubation with EDDF in the L-NNA group (13.0 +/- 0.9 vs 13.2 +/- 0.3 and 148 +/- 16 vs 186 +/- 12). The cGMP level (pmol/g) of aorta in L-NNA group were obviously lower than that of control rats (148 +/- 16 vs 186 +/- 12, P < 0.05). Immunohistological staining of NOS in aorta was obviously lighter in L-NNA group than in control group. The immunohistochemical staining intensity in aorta remained the same after incubation with EDDF in L-NNA group.

The NO/cGMP pathway might be in charge of vasodilation mechanism of EDDF.