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Tacrolimus Causes Hypertension by Increasing Vascular Contractility via RhoA (Ras Homolog Family Member A)/ROCK (Rho-Associated Protein Kinase) Pathway in Mice
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- Wang, Xiaohua (författare)
- Sun Yat Sen Univ, Affiliated Hosp 7, Ctr Kidney & Urol, Dept Nephrol, Shenzhen, Peoples R China.
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- Jiang, Shan (författare)
- Sun Yat Sen Univ, Affiliated Hosp 7, Ctr Kidney & Urol, Dept Nephrol, Shenzhen, Peoples R China.
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- Fei, Lingyan (författare)
- Sun Yat Sen Univ, Affiliated Hosp 7, Ctr Kidney & Urol, Dept Nephrol, Shenzhen, Peoples R China.
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- Sun Yat Sen Univ, Affiliated Hosp 7, Ctr Kidney & Urol, Dept Nephrol, Shenzhen, Peoples R China Zhejiang Univ, Sch Med, Sch Basic Med Sci, Dept Physiol, Hangzhou, Peoples R China. (creator_code:org_t)
- Ovid Technologies (Wolters Kluwer Health), 2022
- 2022
- Engelska.
- Ingår i: Hypertension. - : Ovid Technologies (Wolters Kluwer Health). - 0194-911X .- 1524-4563. ; 79:10, s. 2228-2238
- Tidskriftsartikel (refereegranskat)
Abstract
Ämnesord
Stäng
- Background: To provide tacrolimus is first-line treatment after liver and kidney transplantation. However, hypertension and nephrotoxicity are common tacrolimus side effects that limit its use. Although tacrolimus-related hypertension is well known, the underlying mechanisms are not. Here, we test whether tacrolimus-induced hypertension involves the RhoA (Ras homolog family member A)/ROCK (Rho-associated protein kinase) pathway in male C57Bl/6 mice. methods: Intra-arterial blood pressure was measured under anesthesia. The reactivity of renal afferent arterioles and mesenteric arteries were assessed in vitro using microperfusion and wire myography, respectively. Results: Tacrolimus induced a transient rise in systolic arterial pressure that was blocked by the RhoA/ROCK inhibitor Fasudil (12.0 +/- 0.9 versus 3.2 +/- 0.7; P<0.001). Moreover, tacrolimus reduced the glomerular filtration rate, which was also prevented by Fasudil (187 +/- 20 versus 281 +/- 8.5; P<0.001). Interestingly, tacrolimus enhanced the sensitivity of afferent arterioles and mesenteric arteries to Ang II (angiotensin II), likely due to increased intracellular Ca2+ mobilization and sensitization. Fasudil prevented increased Ang II-sensitivity and blocked Ca2+ mobilization and sensitization. Preincubation of mouse aortic vascular smooth muscle cells with tacrolimus activated the RhoA/ROCK/MYPT-1 (myosin phosphatase targeting subunit 1) pathway. Further, tacrolimus increased cytoplasmic reactive oxygen species generation in afferent arterioles (107 +/- 5.9 versus 163 +/- 6.4; P<0.001) and in cultured mouse aortic vascular smooth muscle cells (100 +/- 7.5 versus 160 +/- 23.2; P<0.01). Finally, the reactive oxygen species scavenger Tempol inhibited tacrolimus-induced Ang II hypersensitivity in afferent arterioles and mesenteric arteries. Conclusions: The RhoA/ROCK pathway may play an important role in tacrolimus-induced hypertension by enhancing Ang II-specific vasoconstriction, and reactive oxygen species may participate in this process by activating the RhoA/ROCK pathway.
Ämnesord
- MEDICIN OCH HÄLSOVETENSKAP -- Klinisk medicin -- Kardiologi (hsv//swe)
- MEDICAL AND HEALTH SCIENCES -- Clinical Medicine -- Cardiac and Cardiovascular Systems (hsv//eng)
Nyckelord
- angiotensin II
- hypertension
- reactive oxygen species
- tacrolimus
- vasoconstriction
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- Wang, Xiaohua
- Jiang, Shan
- Fei, Lingyan
- Dong, Fang
- Xie, Lanyu
- Qiu, Xingyu
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- Lei, Yan
- Guo, Jie
- Zhong, Ming
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