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<p>The skin has recently been highlighted as a new player regulating blood pressure (BP). Here we show the role of skin renin-angiotensin system (RAS) in hypertension. In human subjects, skin expression of angiotensin II (Ang II) type 1 receptor (AT1R)-associated protein (ATRAP), which inhibits pathological AT1R signaling, is inversely correlated with systolic BP. Keratinocyte-specific ATRAP knockout male mice (KO) exhibit exacerbated Ang II-induced hypertension and skin-specific increases in angiotensinogen and Ang II levels. In keratinocyte-specific ATRAP and AT1R knockout male mice, Ang II-induced skin angiotensinogen excess and exaggerated hypertension seen in KO are eliminated. Although body fluid volume is comparable between the genotypes, the urine volume per water intake in Ang II-infused KO is increased, suggesting decreased extra-renal water loss, which is supported by decreased skin blood flow and transepidermal water loss in KO. Body temperature elevation-induced skin vasodilation eliminates these differences, including exaggerated hypertension, indicating the contribution of skin RAS-mediated vasoconstriction to BP elevation. Skin RAS may become a potential strategy for therapeutic interventions in hypertension.</p>

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Keratinocyte-specific angiotensin II receptor-associated protein deficiency exacerbates angiotensin II-dependent hypertension via activation of the skin renin-angiotensin system

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年5月29日

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  • Shinya Taguchi,
  • Kengo Azushima,
  • Kento Kitada,
  • Norihiko Morisawa,
  • Satoshi Kidoguchi,
  • Ryutaro Morita,
  • Kazuya Nakagawa,
  • Atsushi Ishibe,
  • Itaru Endo,
  • Keisuke Kazama,
  • Yasushi Rino,
  • Aya Saito,
  • Sho Kinguchi,
  • Ryu Kobayashi,
  • Taiji Matsusaka,
  • Akio Yamashita,
  • Hiromichi Wakui,
  • Akira Nishiyama,
  • Kouichi Tamura

摘要

The skin has recently been highlighted as a new player regulating blood pressure (BP). Here we show the role of skin renin-angiotensin system (RAS) in hypertension. In human subjects, skin expression of angiotensin II (Ang II) type 1 receptor (AT1R)-associated protein (ATRAP), which inhibits pathological AT1R signaling, is inversely correlated with systolic BP. Keratinocyte-specific ATRAP knockout male mice (KO) exhibit exacerbated Ang II-induced hypertension and skin-specific increases in angiotensinogen and Ang II levels. In keratinocyte-specific ATRAP and AT1R knockout male mice, Ang II-induced skin angiotensinogen excess and exaggerated hypertension seen in KO are eliminated. Although body fluid volume is comparable between the genotypes, the urine volume per water intake in Ang II-infused KO is increased, suggesting decreased extra-renal water loss, which is supported by decreased skin blood flow and transepidermal water loss in KO. Body temperature elevation-induced skin vasodilation eliminates these differences, including exaggerated hypertension, indicating the contribution of skin RAS-mediated vasoconstriction to BP elevation. Skin RAS may become a potential strategy for therapeutic interventions in hypertension.