Abstract:
Background: The reduced level of oxidative stress in RVLM decreased blood pressure (BP), emphasized the dominant role of oxidative stress in pathogenesis of hypertension. This effect on the sympathetic regulation was described in this study as to compare BP response to glutamate (Glu) microinjection into RVLM between SHRSP and SHR.

Methods: We measured oxidative stress level in RVLM of SHRSP and SHR. Microinjection  was conducted using Glu, Glu+losartan and Glu+tempol into the RVLM of SHRSP, SHR and  a congenic strain SP.MES (p22phox knock-out in SHRSP). BP was recorded and urinary norepinephrine (u-NE) was quantified under cold stress (4degree celcius).

Results: Oxidative stress level was significantly higher in SHRSP compared to SHR. In response to RVLM microinjection of Glu, BP was increased abruptly in SHRSP compared to SHR; inhibition of this response was also observed (using losartan and tempol) only in SHRSP. Besides, SHRSP showed higher baseline BP and subsequently increased effect under cold stress. SP.MES showed similar effect like SHR.

Conclusion: We observed that BP response to Glu might mostly be influenced by the abnormal activation of NOX in SHRSP. And, if so, SHRSP might depend on this influence for high baseline BP and exaggerated stress response; to activate glutamatergic neurons in RVLM, and AT1R might be involved in this process. The results suggested that the NOX channel in SHR may not as strong as SHRSP to stimulate Glu in RVLM neurons.

BLOOD PRESSURE RESPONSE TO GLUTAMATE MICROINJECTION INTO RVLM WAS GREATER IN SHRSP THAN IN SHR, WHICH MIGHT BE DUE TO THE EXAGGERATED NADPH OXIDASE ACTIVITY