scholarly journals Race/ethnicity determines the relationships between oxidative stress markers and blood pressure in individuals with high cardiovascular disease risk

2016 ◽  
Vol 31 (1) ◽  
pp. 70-75 ◽  
Author(s):  
G Kapuku ◽  
F Treiber ◽  
F Raouane ◽  
J Halbert ◽  
H Davis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Oxidative Stress Markers ◽  
Stress Markers ◽  
Race Ethnicity

Abstract 1378: NFkb Blockade Attenuate Cytokines And Oxidative Stress In The Paraventricular Nucleus And Decreases Neurohumoral Excitation In Spontaneously Hypertensive Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Nithya Mariappan ◽  
Carrie Elks ◽  
Masudul Haque ◽  
Philip J Ebnezer ◽  
Elizabeth McIIwain ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Paraventricular Nucleus ◽  
Spontaneously Hypertensive Rats ◽  
Left Ventricular ◽  
Oxidative Stress Markers ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Stress Markers ◽  
And Oxidative Stress

The transcriptional factor, nuclear factor kappa B (NFkB) plays an important role in the regulation of cytokines. Among the cytokines, tumor necrosis factor-alpha (TNF) plays an important role in cardiovascular pathophysiology. This study was done to determine whether TNF-α blockade with etanercept (ETN) or NFkB blockade with dithiol pyrolidine thiocarbamate (PDTC) attenuate oxidative stress in the paraventricular nucleus (PVN) and contribute to neurohumoral excitation in spontaneously hypertensive rats. Method: Male 20 week old SHR rats were treated with ETN (1 mg/kg BW, sc) or PDTC (100mg/kg BW, ip) for 5 week period. Left ventricular function was measured at baseline (20 weeks) and at 25 weeks using echocardiography. Blood pressure was measured at weekly intervals throughout the study. At the end of the protocol rats were sacrificed the PVN was microdissected for the measurement of cytokines, oxidative stress markers using real time PCR (fold increase compared to WKY controls) and by immunohistochemistry. Superoxide, total reactive oxygen species and peroxynitrite were measured in the PVN and LV using electron paramagnetic resonance. Plasma norepinephrine and epinephrine an indicator of neurohumoral excitation was measured using HPLC-EC. Results: PVN data are tabulated. SHR animals had increased expression of protein and mRNA for cytokines and oxidative stress markers in the PVN and LV with increased MAP and cardiac hypertrophy when compared to WKY rats. Treatment with ETN and PDTC attenuated these increases with PDTC showing marked effect than ETN on hypertrophy and blood pressure responses. Conclusion: These findings suggest that cytokine activation in the PVN contributes to increased oxidative stress and neurohumoral excitation in hypertension.

Abstract P081: Tempol Decreases Blood Pressure in Aged Female SHR When Treated With Acetazolamide

Hypertension ◽  
2015 ◽  
Vol 66 (suppl_1) ◽  
Author(s):  
Carolina Dalmasso ◽  
Rodrigo O Maranon ◽  
Chetan N Patil ◽  
Andrew Harris ◽  
Huimin Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Young Male ◽  
Sodium Reabsorption ◽  
Oxidative Stress Markers ◽  
Distal Nephron ◽  
Stress Markers ◽  
Total Antioxidant ◽  
Sodium Handling ◽  
Lucigenin Chemiluminescence

Oxidative stress contributes to the development and maintenance of hypertension in male rodents, but studies in females have rarely shown a reduction in blood pressure (BP) with antioxidants. Tempol, a superoxide dismutase mimetic, decreases BP in young male SHR, but fails to reduce BP in either young or old female SHR, despite the fact that females have similar or higher levels of oxidative stress markers. The reason for the sex difference in the response to tempol remains unclear. Acetazolamide inhibits carbonic anhydrase in the proximal tubule thus increasing sodium delivery to the distal nephron, and thereby should increase distal oxidative stress. Acetazolamide was used to test the hypothesis that with increased sodium delivery to the distal nephron, tempol would reduce the BP in aging female SHR. Female SHR, 20-22 mos old, were divided into three groups (n=4-6/grp): Control (C), Acetazolamide (A), and Acetazolamide+Tempol (A+T). After baseline mean arterial pressure (MAP; telemetry), rats received vehicle (C) or acetazolamide (A and A+T). On day 8, rats in C and A+T groups were given tempol (30 mg/kg) for 11 days. Baseline MAP was similar (C: 170±7; A: 182±4; A+T: 172±6 mm Hg, p=NS). Tempol had no effect on MAP in C+T, but reduced MAP in A+T group (C+T: 169±1; A: 171±1; A+T: 151±5 mm Hg; p<0.005 A+T vs A, C+T). Basal renal oxidative stress measured by lucigenin chemiluminescence was not different in the groups; NADPH-stimulated oxidative stress was decreased in A+T compared to A and C+T (C+T: 641.8±72.2; A: 499.3±18.3; A+T: 406.2±56.3 RLU/mg/min; p<0.05, A+T vs A, C+T). Plasma total antioxidant capacity was increased by tempol only in A+T rats (C+T: 59.07±9.67; A: 69.01±4.66; A+T: 118.24±18.38 nmol/μl; p<0.05, A+T vs A, C+T). Thus tempol is capable of modestly reducing MAP in aging female SHR when proximal sodium reabsorption is blocked. The data suggest that oxidative stress-mediated BP control is dependent on increased sodium delivery to the distal nephron. Because hypertension in male SHR is attenuated with tempol alone, but not in females, taken together, the data suggest sex differences in sodium handling and thus localization of oxidative stress production in the kidneys of SHR. Supported by NIH-R01HL66072, PO1HL51971 (JFR), 14POST18640015 (ROM).

scholarly journals Age modification of ozone associations with cardiovascular disease risk in adults: a potential role for soluble P-selectin and blood pressure

2018 ◽  
Vol 10 (7) ◽  
pp. 4643-4652 ◽  
Author(s):  
Drew B. Day ◽  
Merlise A. Clyde ◽  
Jianbang Xiang ◽  
Feng Li ◽  
Xiaoxing Cui ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Potential Role ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Soluble P

scholarly journals Vitamin D Receptor Activation Mitigates the Impact of Uremia on Endothelial Function in the 5/6 Nephrectomized Rats

2010 ◽  
Vol 2010 ◽  
pp. 1-10 ◽  
Author(s):  
J. Ruth Wu-Wong ◽  
William Noonan ◽  
Masaki Nakane ◽  
Kristin A. Brooks ◽  
Jason A. Segreti ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Cardiovascular Disease ◽  
Chronic Kidney Disease ◽  
Heart Rate ◽  
Vitamin D ◽  
Endothelial Function ◽  
Disease Risk ◽  
Cardiovascular Disease Risk ◽  
Receptor Activation ◽  
The Impact

Endothelial dysfunction increases cardiovascular disease risk in chronic kidney disease (CKD). This study investigates whether VDR activation affects endothelial function in CKD. The 5/6 nephrectomized (NX) rats with experimental chronic renal insufficiency were treated with or without paricalcitol, a VDR activator. Thoracic aortic rings were precontracted with phenylephrine and then treated with acetylcholine or sodium nitroprusside. Uremia significantly affected aortic relaxation (% in NX rats versus % in SHAM at 30 M acetylcholine). The endothelial-dependent relaxation was improved to –%, –%, and –% in NX rats treated with paricalcitol at 0.021, 0.042, and 0.083 g/kg for two weeks, respectively, while paricalcitol at 0.042 g/kg did not affect blood pressure and heart rate. Parathyroid hormone (PTH) suppression alone did not improve endothelial function since cinacalcet suppressed PTH without affecting endothelial-dependent vasorelaxation. N-omega-nitro-L-arginine methyl ester completely abolished the effect of paricalcitol on improving endothelial function. These results demonstrate that VDR activation improves endothelial function in CKD.

Sign in / Sign up

Export Citation Format

Share Document