The effect of maintenance and reversal of DOCA-Salt hypertension on extravasation of macromolecules and serum nitric oxide concentration in male rats

Objective: Previous studies indicated that there are some functional and morphological changes of endothelial cells in hypertension. The aim of this study was to investigate the effect of DOCA-Salt hypertension and its reversal on extravasation of macromolecules (endothelial permeability) and serum Nitric Oxide (NO) concentrations in male rats. Method: Male rats were divided into four groups as follows: Group (i): DOCA-Salt for 12 weeks; Group (ii): Solvent of DOCA injection for 12 weeks; Group (iii): DOCA-Salt for 12 weeks and DOCA-Salt withdrawal for 12 weeks; Group (iv): Solvent of DOCA injection for 12 weeks and its withdrawal for 12 weeks. At the end of experiment, serum NO concentrations were measured and vascular permeability in aorta and coronary circulation were evaluated using Evans Blue dye method. Results: Results showed that systolic blood pressure was significantly higher in DOCA-Salt hypertensive rats compared to normotensive group (150.1 ± 2.42 vs. 97.7 ± 2.32 mmHg, respectively). DOCA-Salt withdrawal completely reduced blood pressure in hypertensive rats to normotensive level (150.1 ± 2.42 vs. 98.1 ± 3.68 mmHg, respectively). Coronary vascular and aortic endothelial permeability were not different between DOCA-Salt hypertensive and normotensive rats and reversal of blood pressure did not alter it. Serum NO level was significantly lower in the hypertensive animals compared to normotensive group (3.87 ± 0.97 vs. 7.71 ± 0.67 μmol/l) and blood pressure reduction returned serum NO level to normotensive level (7.25 ± 0.96 vs. 7.71 ± 0.67 μmol/l). Conclusion: DOCA-Salt hypertension and its reversal did not alter coronary vascular and aortic endothelial permeability. However, serum NO level was significantly reduced during hypertension and reversal of hypertension completely reduced blood pressure together with the restoration of serum NO concentration. This may suggest that biological marker of endothelial function do not behave uniformly at least in this model of hypertension.