Effect of tumor necrosis factor-α inhibitors on ambulatory 24-h blood pressure

2016 ◽  
Vol 26 (1) ◽  
pp. 24-29 ◽  
Author(s):  
Chagai Grossman ◽  
Gil Bornstein ◽  
Avshalom Leibowitz ◽  
Ilan Ben-Zvi ◽  
Ehud Grossman
Keyword(s):  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor Necrosis Factor-α Antagonist Etanercept Decreases Blood Pressure and Protects the Kidney in a Mouse Model of Systemic Lupus Erythematosus

Hypertension ◽  
2010 ◽  
Vol 56 (4) ◽  
pp. 643-649 ◽  
Author(s):  
Marcia Venegas-Pont ◽  
Michaele B. Manigrasso ◽  
Samira C. Grifoni ◽  
Babbette B. LaMarca ◽  
Christine Maric ◽  
...  
Keyword(s):  
Systemic Lupus Erythematosus ◽  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
Mouse Model ◽  
Lupus Erythematosus ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Systemic Lupus ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Tumor necrosis factor-α: regulation of renal function and blood pressure

2013 ◽  
Vol 304 (10) ◽  
pp. F1231-F1242 ◽  
Author(s):  
Vanesa D. Ramseyer ◽  
Jeffrey L. Garvin
Keyword(s):  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Immune Cell ◽  
Organ Damage ◽  
Physiological Status ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Tumor necrosis factor-α (TNF-α) is a pleiotropic cytokine that becomes elevated in chronic inflammatory states such as hypertension and diabetes and has been found to mediate both increases and decreases in blood pressure. High levels of TNF-α decrease blood pressure, whereas moderate increases in TNF-α have been associated with increased NaCl retention and hypertension. The explanation for these disparate effects is not clear but could simply be due to different concentrations of TNF-α within the kidney, the physiological status of the subject, or the type of stimulus initiating the inflammatory response. TNF-α alters renal hemodynamics and nephron transport, affecting both activity and expression of transporters. It also mediates organ damage by stimulating immune cell infiltration and cell death. Here we will summarize the available findings and attempt to provide plausible explanations for such discrepancies.

Tumor necrosis factor-α-angiotensin interactions and regulation of blood pressure

1997 ◽  
Vol 15 (12) ◽  
pp. 1481-1484 ◽  
Author(s):  
Nicholas R. Ferreri ◽  
Yejun Zhao ◽  
Hideki Takizawa ◽  
John C. McGiff
Keyword(s):  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Regulation Of Blood Pressure ◽  
Necrosis Factor

scholarly journals Central Leptin and Tumor Necrosis Factor-α (TNFα) in Diurnal Control of Blood Pressure and Hypertension

2016 ◽  
Vol 291 (29) ◽  
pp. 15131-15142 ◽  
Author(s):  
Cheng Han ◽  
Wenhe Wu ◽  
Albert Ale ◽  
Min Soo Kim ◽  
Dongsheng Cai
Keyword(s):  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Factor Α ◽  
Necrosis Factor

scholarly journals Oxidative stress and biomarker of TNF-α, MDA and FRAP in hypertension

2019 ◽  
Vol 12 (3) ◽  
pp. 253-259 ◽  
Author(s):  
Manish Kumar Verma ◽  
◽  
Anoop Jaiswal ◽  
Preeti Sharma ◽  
Pradeep Kumar ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Pressure ◽  
Tumor Necrosis Factor ◽  
High Blood Pressure ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Hypertensive Patients ◽  
Tnf Α ◽  
Factor Α ◽  
Necrosis Factor

Concurrent with the misbalance of oxidizing agents and antioxidants, high blood pressure is a major physical burden condition in the current scenario. Tumor necrosis factor-α (TNF-α) plays a vital role in the pathogenesis of hypertension. Tumor necrosis factor-α, inhibitor improves clinical symptoms however their outcome on high blood pressure has not been investigated. We investigated the inflammatory marker TNF-α, malondialdehyde (MDA) and ferric reducing antioxidant power (FRAP) in hypertensive patients. We measured randomly blood pressure using an ambulatory observe in hypertensive patients, measured systolic BP X 140 mmHg and/or diastolic BP X 90 mmHg were considered hypertensive. Total 60 cases were considered in the study that involves 30 hypertensive patients and 30 normal control. Measurements of serum concentrations of TNF-α, MDA, FRAP in hypertension patients was done in both the groups. Serum TNF-α was found to be remarkably increased in study subjects as compared to normal group (r=0.32, p<0.0001*). Serum MDA was also raised in hypertensive as compared to control (r=0.99**, p<0.0001*). While Serum FRAP was found to be decreased in hypertensive group in comparison to healthy control (r=0.23, p<0.0001*). It is concluded that high blood pressure leads to generation of oxidative stress with remarkable elevation of TNF-α and malondialdehyde levels. While reduced FRAP indicates its probable role in lipid peroxidation and in the pathogenesis of hypertension.

scholarly journals Chronic hyperleptinemia results in the development of hypertension in pregnant rats

2015 ◽  
Vol 308 (10) ◽  
pp. R855-R861 ◽  
Author(s):  
Ana C. Palei ◽  
Frank T. Spradley ◽  
Joey P. Granger
Keyword(s):  
Blood Pressure ◽  
Body Weight ◽  
Food Intake ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Α ◽  
Pregnant Rats ◽  
Ad Libitum ◽  
Factor Α ◽  
Necrosis Factor

Despite the fact that obesity is a major risk factor for preeclampsia (PE), the pathophysiological mechanisms whereby obesity and metabolic factors such as leptin increase this risk are unclear. While human data have shown that hyperleptinemia is associated with PE, the long-term effect of hyperleptinemia on blood pressure during pregnancy is unknown. Thus we tested the hypothesis whether chronic circulating leptin elevations in pregnant rats increase blood pressure and placental factors known to play a role in PE. On gestational day (GD)14, rats were assigned to the normal pregnant group with food intake ad libitum (control), leptin-treated (0.5 μg·kg−1·min−1 ip) pregnant group with food intake ad libitum (pregnant+LEP), and normal pregnant group with food intake adjusted to the food intake of pregnant+LEP rats (pregnant-FR). On GD19, mean arterial pressure (MAP) was assessed and tissues were collected. Serum leptin concentration was elevated in pregnant+LEP compared with control and pregnant-FR (18.0 ± 2.8 vs. 0.8 ± 0.1 vs. 0.3 ± 0.1 ng/ml; P < 0.05), which was associated with increased MAP (121.3 ± 8.1 vs. 102.4 ± 2.4 vs. 101.3 ± 1.8 mmHg; P < 0.05). Food intake and body weight were reduced in pregnant+LEP and pregnant-FR by the end of gestation. Additionally, placentas and fetuses of these groups were lighter than those of control. However, placental expression of tumor necrosis factor-α was significantly greater in pregnant+LEP compared with controls (1.6 ± 0.1 vs. 1.1 ± 0.1 pg/mg; P < 0.05). In conclusion, leptin increases blood pressure and placental tumor necrosis factor-α during pregnancy despite its effect of reducing food intake and body weight, and represents a mechanism whereby obesity can promote the development of hypertension in PE.

Sign in / Sign up

Export Citation Format

Share Document