Affiliations: Departments of Physiology, Biochemistry and Pharmacology, Akdeniz University Medical Faculty, Antalya, Turkey
Note: [] Deceased.
Note: [] Corresponding author: Oguz K. Başkurt, MD, PhD. Department of Physiology, Akdeniz University Faculty of Medicine, Kampus, Antalya, Turkey. Fax: +90 242 227 4463, E‐mail: baskurt@akdeniz.edu.tr.
Abstract: Nitric oxide (NO) plays a major role in vascular regulation. Modulation of NO synthesis is known to influence blood pressure. Inhibition of NO synthesis 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 aggregation measured in autologous plasma, by a photometric rheoscope also increased significantly in the hypertensive rats. RBC cytosolic free calcium concentration was also significantly higher in the hypertensive animals. Incubation of RBC from hypertensive and control animals with NO donor, sodium nitroprussid (SNP; 10–1000 μM) for 60 minutes resulted in a dose‐dependent decrease in RBC aggregation, however aggregation index was significantly higher in hypertensive group at each SNP concentration. Incubation with SNP had no effect on RBC deformability in the control group, while a slight decrease in RBC transit time was observed only at 10 μM SNP in the hypertensive group. These results imply that NO may play a role in the regulation of rheological properties of RBC and the alterations in these properties may at least in part be involved in the development of L‐NAME induced hypertension.
