Key result
TNF-α exerts dose-dependent blood pressure effects, lowering pressure at high levels and raising it at moderate levels.
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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.
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Ramseyer et al. (2013) conducted a review in Hypertension and chronic inflammatory states. Tumor necrosis factor-α (TNF-α) was evaluated. Tumor necrosis factor-α has disparate effects, with high levels decreasing and moderate levels increasing blood pressure via altered renal hemodynamics, NaCl retention, and nephron transport.
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