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Impact of 12 wks Exercise on Renal Nitric Oxide and Antioxidant Status: A Strain Difference Comparison
Author(s) -
Moningka Natasha,
Cunningham Mark,
Sterling Myrline,
Baylis Chris
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.1059.1
Subject(s) - enos , oxidative stress , medicine , endocrinology , nitric oxide , ex vivo , superoxide dismutase , nitric oxide synthase , chemistry , p22phox , nitric oxide synthase type iii , reactive oxygen species , antioxidant , superoxide , nadph oxidase , biochemistry , enzyme , in vitro
One mechanism by which the vasculature benefits from exercise (EX) is by increases in blood flow (BF). This causes increases in shear stress and induction of the endothelial nitric oxide synthase (eNOS) and antioxidant, extracellular superoxide dismutase (EC SOD). The kidney, however, undergoes reduced BF during EX and therefore may be at risk for falls in NO and antioxidant bioavailability. Genetic differences may also dictate this response. Therefore, we investigated kidney cortex (KC) responses to EX in the Sprague Dawley (SD) and Fisher 344 (F344) rat. Male SD and F344 rats (10–12 wks old) voluntarily wheel ran for 12 wks (24 hr access) or remained sedentary (SED). Running activity was similar between strains. Nitrate/nitrite (NOx) levels and eNOS and EC SOD abundance in the KC of F344 rats increased with EX ( Table; *p≤0.05 vs. SED). In contrast, SD rats decreased their renal eNOS and EC SOD with no change in KC NOx. The oxidative stress marker p22phox also increased in the KC of EX F344 but decreased in the EX SD rat. Another oxidative stress marker, H 2 O 2 , measured in KC, increased only in EX F344 rats. These findings indicate that a strain difference exists in the response to 12 wks voluntary EX between the F344 and SD rat. F344 rats increased their KC eNOS and EC SOD and this was interestingly also associated with increased oxidative stress. Conversely, SD rats had the opposite response to EX in their KC: reduced eNOS and EC SOD and either decreased p22phox or no change in H 2 O 2 . Mechanisms responsible for these marked differences in renal responses to EX remain to be determined.eNOS NOx EC SOD p22phox H 2 O 2n Arbitrary Units nmol/mg Arbitrary Units Arbitrary Units nmol/mgF344SED 12 6±1.2 8±1.7 68±23 5±0.5 0.2±0.04 EX 12 18±3.2* 15±6.3* 122±27* 8±0.6* 0.6±0.14*SDSED 6 64±2.6 9±0.4 13±1.0 9±0.4 0.4±0.07 EX 6 56±2.2* 10±0.4 8±0.7* 7±0.6* 0.5±0.07