https://wiki.tiffa.net/w/index.php?action=history&feed=atom&title=Translations%3AHypertension%2F26%2FenTranslations:Hypertension/26/en - Revision history2026-09-15T11:44:43ZRevision history for this page on the wikiMediaWiki 1.43.0https://wiki.tiffa.net/w/index.php?title=Translations:Hypertension/26/en&diff=123469&oldid=prevFuzzyBot: Importing a new version from external source2024-02-29T13:03:01Z<p>Importing a new version from external source</p>
<p><b>New page</b></p><div>Many mechanisms have been proposed to account for the rise in peripheral resistance in hypertension. Most evidence implicates either disturbances in the kidneys' salt and water handling (particularly abnormalities in the intrarenal [[renin–angiotensin system]]) or abnormalities of the [[sympathetic nervous system]]. These mechanisms are not mutually exclusive and it is likely that both contribute to some extent in most cases of essential hypertension. It has also been suggested that [[endothelial dysfunction]] and vascular [[inflammation]] may also contribute to increased peripheral resistance and vascular damage in hypertension. [[Interleukin 17]] has garnered interest for its role in increasing the production of several other [[cytokine|immune system chemical signals]] thought to be involved in hypertension such as [[tumor necrosis factor alpha]], [[interleukin 1]], [[interleukin 6]], and [[interleukin 8]].</div>FuzzyBot