Ni Wei, Zhou Huawei, Diaz Jessica, Murphy Dennis L, Haywood Joseph R, Watts Stephanie W
Department of Pharmacology and Toxicology, Michigan State University, East Lansing, MI 48824-1317, USA.
Eur J Pharmacol. 2008 Jul 28;589(1-3):225-7. doi: 10.1016/j.ejphar.2008.06.012. Epub 2008 Jun 7.
We hypothesized that lack of a functional serotonin transporter (SERT) would increase basal blood pressure and enhance the development of deoxycorticosterone acetate (DOCA)-salt hypertension compared to wild type (WT) controls. Mean arterial blood pressure was measured in WT and SERT knockout (KO) mice and rat models through radiotelemetry. Basal blood pressures were not different between respective WT and KO. Moreover, blood pressure elevated similarly (~50 mm Hg) in all strains given DOCA and salt. Thus, the lack of functional SERT did not prevent development of DOCA-salt induced hypertension or modify basal blood pressure significantly.
我们推测，与野生型（WT）对照相比，缺乏功能性5-羟色胺转运体（SERT）会升高基础血压，并增强醋酸脱氧皮质酮（DOCA）-盐性高血压的发展。通过无线电遥测技术在WT和SERT基因敲除（KO）小鼠及大鼠模型中测量平均动脉血压。各WT和KO之间的基础血压并无差异。此外，给予DOCA和盐后，所有品系的血压均以相似幅度升高（约50 mmHg）。因此，功能性SERT的缺乏并未阻止DOCA-盐诱导的高血压的发展，也未显著改变基础血压。
