Red blood cell rheological alterations in hypertension induced by chronic inhibition of nitric oxide synthesis in rats

Nitric oxide (NO) plays a major role in vascular regulation. Modulation of NO synthesis is known to influence blood pressure. Inhibition of NO synthes is by NG-nitro-L-arginine methyl ester (L-NAME; 72 mg/kg/day, p.o., 21 days ) resulted in 60% increase in blood pressure in rats. Red blood cell (RBC) transit time measured by the cell transit analyzer increased significantly in the L-NAME treated group, in comparison to normotensive rats. RBC aggreg ation measured in autologous plasma, by a photometric rheoscope also increa sed significantly in the hypertensive rats. RBC cytosolic free calcium conc entration was also significantly higher in the hypertensive animals. Incuba tion of RBC from hypertensive and control animals with NO donor, sodium nit roprussid (SNP; 10-1000 mu M) for 60 minutes resulted in a dose-dependent d ecrease in RBC aggregation, however aggregation index was significantly hig her in hypertensive group at each SNP concentration. Incubation with SNP ha d no effect on RBC deformability in the control group, while a slight decre ase in RBC transit time was observed only at 10 mu M SNP in the hypertensiv e group. These results imply that NO may play a role in the regulation of r heological properties of RBC and the alterations in these properties may at least in part be involved in the development of L-NAME induced hypertensio n.