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1 Department of Physiology and Biophysics, University of Mississippi Medical Center, Jackson, MS, USA
* To whom correspondence should be addressed. E-mail: jreckelhoff{at}physiology.umsmed.edu.
Spontaneously hypertensive rats (SHR) have a higher level of oxidative stress and exhibit a greater depressor response to a superoxide scavenger, tempol, than normotensive WKY rats. This study determined whether an increase in oxidative stress with a superoxide/nitric oxide (NO) donor, molsidomine, would amplify the blood pressure in SHR. Male SHR and WKY were given molsidomine (30 mg/kg/d) or vehicle (0.01% ethanol) for 1 week, and blood pressure, renal hemodynamics, nitrate and nitrite excretion (NOx), renal superoxide production and expression of renal antioxidant enzymes, Mn- and Cu,Zn-SOD, catalase and glutathione peroxidase (GPx), were measured. Renal superoxide and NOx were higher in control SHR than in WKY. Molsidomine increased superoxide by approximately 35% and NOx by 250% in both SHR and WKY. Mean arterial blood pressure (MAP) was also higher in control SHR than WKY. Molsidomine increased MAP by 14% and caused renal vasoconstriction in SHR, but reduced MAP by 16%) with no effect on renal hemodynamics in WKY. Renal expression of Mn- and Cu,Zn-SOD was not different between SHR and WKY, but expression of catalase and glutathione peroxidase were approximately 30% lower in kidney of SHR than WKY. The levels of Mn- and Cu,Zn-SOD were not increased with molsidomine in either WKY or SHR. In WKY, renal catalase and GPx expression was increased by 300-400% with molsidomine, but there was no effect in SHR. Increasing oxidative stress elevated blood pressure further in SHR, but not WKY. The WKY are likely protected due to higher bioavailable levels of NO and the ability to upregulate catalase and GPx.
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