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We began analyzing https://link.springer.com/article/10.1007/s11906-018-0903-x, but it redirected us to https://link.springer.com/article/10.1007/s11906-018-0903-x. The analysis below is for the second page.

Title[redir]:
Inflammation in Salt-Sensitive Hypertension and Renal Damage | Current Hypertension Reports
Description:
Purpose of Review Low-grade inflammation drives elevations in blood pressure (BP) and consequent target organ damage in diverse experimental models of hypertension. Here, we discuss recent advances elucidating immune-mediated mechanisms of BP elevation and associated target organ damage. Recent Findings Inflammatory mediators produced by immune cells or target organs act on the kidney, vasculature, skin, and nervous system to modulate hypertension. For example, cells of the innate immune system, including monocytes, neutrophils, and dendritic cells (DCs), can all promote BP elevation via actions in the vasculature and kidney. Macrophages expressing VEGF-C impact non-osmotic sodium storage in the skin that in turn regulates salt sensitivity. Within the adaptive immune system, activated T cells can secrete tumor necrosis factor-alpha (TNF-α), interleukin-17a (IL-17a), and interferon-gamma (IFN-γ), each of which has augmented BP and renal damage in pre-clinical models. Inversely, deficiency of IL-17a in mice blunts the hypertensive response and attenuates renal sodium retention via a serum- and glucocorticoid-regulated kinase 1 (SGK1)–dependent pathway. Linking innate and adaptive immune responses, dendritic cells activated by augmented extracellular sodium concentrations stimulate T lymphocytes to produce pro-hypertensive cytokines. By contrast, regulatory T cells (Tregs) can protect against hypertension and associated kidney injury. Summary Rodent studies reveal diverse mechanisms via which cells of the innate and adaptive immune systems drive blood pressure elevation by altering the inflammatory milieu in the kidney, vasculature, and brain.

Matching Content Categories {📚}

  • Health & Fitness
  • Science
  • Education

Content Management System {📝}

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Custom-built

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Keywords {🔍}

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Topics {✒️}

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Questions {❓}

  • Do statins reduce blood pressure?
  • Increased serum levels of interleukin-1beta in the systemic circulation of patients with essential hypertension: additional risk factor for atherogenesis in hypertensive patients?

Schema {🗺️}

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         headline:Inflammation in Salt-Sensitive Hypertension and Renal Damage
         description:Low-grade inflammation drives elevations in blood pressure (BP) and consequent target organ damage in diverse experimental models of hypertension. Here, we discuss recent advances elucidating immune-mediated mechanisms of BP elevation and associated target organ damage. Inflammatory mediators produced by immune cells or target organs act on the kidney, vasculature, skin, and nervous system to modulate hypertension. For example, cells of the innate immune system, including monocytes, neutrophils, and dendritic cells (DCs), can all promote BP elevation via actions in the vasculature and kidney. Macrophages expressing VEGF-C impact non-osmotic sodium storage in the skin that in turn regulates salt sensitivity. Within the adaptive immune system, activated T cells can secrete tumor necrosis factor-alpha (TNF-α), interleukin-17a (IL-17a), and interferon-gamma (IFN-γ), each of which has augmented BP and renal damage in pre-clinical models. Inversely, deficiency of IL-17a in mice blunts the hypertensive response and attenuates renal sodium retention via a serum- and glucocorticoid-regulated kinase 1 (SGK1)–dependent pathway. Linking innate and adaptive immune responses, dendritic cells activated by augmented extracellular sodium concentrations stimulate T lymphocytes to produce pro-hypertensive cytokines. By contrast, regulatory T cells (Tregs) can protect against hypertension and associated kidney injury. Rodent studies reveal diverse mechanisms via which cells of the innate and adaptive immune systems drive blood pressure elevation by altering the inflammatory milieu in the kidney, vasculature, and brain.
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      headline:Inflammation in Salt-Sensitive Hypertension and Renal Damage
      description:Low-grade inflammation drives elevations in blood pressure (BP) and consequent target organ damage in diverse experimental models of hypertension. Here, we discuss recent advances elucidating immune-mediated mechanisms of BP elevation and associated target organ damage. Inflammatory mediators produced by immune cells or target organs act on the kidney, vasculature, skin, and nervous system to modulate hypertension. For example, cells of the innate immune system, including monocytes, neutrophils, and dendritic cells (DCs), can all promote BP elevation via actions in the vasculature and kidney. Macrophages expressing VEGF-C impact non-osmotic sodium storage in the skin that in turn regulates salt sensitivity. Within the adaptive immune system, activated T cells can secrete tumor necrosis factor-alpha (TNF-α), interleukin-17a (IL-17a), and interferon-gamma (IFN-γ), each of which has augmented BP and renal damage in pre-clinical models. Inversely, deficiency of IL-17a in mice blunts the hypertensive response and attenuates renal sodium retention via a serum- and glucocorticoid-regulated kinase 1 (SGK1)–dependent pathway. Linking innate and adaptive immune responses, dendritic cells activated by augmented extracellular sodium concentrations stimulate T lymphocytes to produce pro-hypertensive cytokines. By contrast, regulatory T cells (Tregs) can protect against hypertension and associated kidney injury. Rodent studies reveal diverse mechanisms via which cells of the innate and adaptive immune systems drive blood pressure elevation by altering the inflammatory milieu in the kidney, vasculature, and brain.
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External Links {🔗}(363)

Analytics and Tracking {📊}

  • Google Tag Manager

Libraries {📚}

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Emails and Hosting {✉️}

Mail Servers:

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Name Servers:

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CDN Services {📦}

  • Crossref

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