Aims:
Vasoconstriction within the renal medulla contributes to the development of hypertension. This study investigated the role of reactive oxygen species (ROS) and nitric oxide (NO) in regulating renal medullary and cortical blood perfusion (MBP and CBP respectively) in stroke prone spontaneously hypertensive rats (SP -SHR)
Methods:
Following anaesthesia, CBP and MBP were measured (laser-Doppler flowmetry) before and after intrarenal infusion of tempol, the superoxide dismutase (SOD) mimetic, tempol, plus the hydrogen peroxide degrading enzyme catalase (tem+cat), diethyldithio-carbamic acid (DETC), a SOD inhibitor, and the nitric oxide synthase (NOS) inhibitor, L-nitro arginine methyl ester (L-NAME).
Results:
Infusion of tempol alone, and co-infusion of catalase and tempol, both significantly elevated MBP by 43±7% (P < 0.01) and 57±7% (P < 0.001), respectively in the SP-SHR rats. DETC infusion on the other hand significantly reduced MBP in these animals by 28±3% (P < 0.05), but had no effect on CBP. L-NAME also significantly reduced MBP in the SP-SHR by 17±5 % (P < 0.05).
Conclusion:
These results suggest that ROS play a greater role in reducing renal vascular compliance than NO, particularly within the medullary region. The effects of ROS are enhanced in these hypertensive animals indicating that the renal vasculature is subjected to elevated oxidative stress.