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【medical-news】噻唑烷二酮类药物降压作用亦与P
5 March 2008
MedWire News: Researchers report that the thiazolidinedione (TZD) target peroxisome proliferator-activated receptor (PPAR)γ plays a pivotal role in vascular smooth muscle cell function and blood pressure regulation.
The results appear to explain why TZDs have been shown to lower blood pressure, as well as reduce blood glucose levels, in Type 2 diabetes patients.
Owing to controversy surrounding possible increased risk for cardiovascular events associated with treatment with the TZD rosiglitazone, Curt Sigmund and colleagues from the University of Iowa in Iowa City, USA, say there is "an urgent need not only to assess the beneficial and consequential effects of TZDs but also to understand the fundamental mechanisms controlling the metabolic and cardiovascular function of PPARγ itself."
As reported in the journal Cell Metabolism, the researchers generated mice expressing high levels of dysfunctional PPARγ, which suppressed normal-function PPARγ. The mice developed high blood pressure levels and severe vascular dysfunction resembling the hallmarks of advanced diabetes.
Aortic tissue taken from these mice showed reduced contractility in response to vasodilating nitric oxide and hypercontractility in response to the potent vasoconstrictor endothelin-1.
Further analysis showed that cerebral arterioles of mice expressing dysfunctional PPARγ underwent hypertrophy, with an increase in distensibility and remodeling and reduction in external diameter.
TZD drugs have some serious side effects including weight gain and fluid retention, as well as increasing the risk for heart failure.
"These side effects really highlight the need to figure out ways to dissociate beneficial effects from dangerous side effects," said Sigmund.
"By understanding the mechanisms that lead to those effects we may be able to enhance benefits and minimize dangers."
The researchers say their next step is to identify which genes are switched on or off downstream of PPARγ to produce the antihypertensive effect, which could lead to more specific interventions to treat hypertension and vascular disease in patients with diabetes.
Cell Metab 2008; 7: 215-226
http://www.incirculation.net/NewsItem/Thiazolidinedione-target-regulates-blood-pressure.aspx Thiazolidinedione target regulates blood pressure
噻唑烷二酮类药物调节血压的靶点
5 March 2008
2008年3月5日
MedWire News: Researchers report that the thiazolidinedione (TZD) target peroxisome proliferator-activated receptor (PPAR)γ plays a pivotal role in vascular smooth muscle cell function and blood pressure regulation.
医学电报新闻：研究者们报道说，噻唑烷二酮类药物的作用靶点过氧化物酶体增殖物激活受体（PPAR）γ对血管平滑肌细胞的功能以及血压的调节有重要作用
The results appear to explain why TZDs have been shown to lower blood pressure, as well as reduce blood glucose levels, in Type 2 diabetes patients.
研究结果解释了，在2型糖尿病患者中，使用噻唑烷二酮类药物降低血糖的同时，也能降低血压。
Owing to controversy surrounding possible increased risk for cardiovascular events associated with treatment with the TZD rosiglitazone, Curt Sigmund and colleagues from the University of Iowa in Iowa City, USA, say there is "an urgent need not only to assess the beneficial and consequential effects of TZDs but also to understand the fundamental mechanisms controlling the metabolic and cardiovascular function of PPARγ itself."
由于目前对噻唑烷二酮类药物可能增加心血管事件的危险性，Curt Sigmund以及他的同事们认为，不仅仅迫切需要评价噻唑烷二酮类药物的利弊，还应进一步明确PPARγ本身的代谢及心血管功能的基础机制。Curt Sigmund目前就职于美国艾奥瓦市的艾奥瓦大学。
As reported in the journal Cell Metabolism, the researchers generated mice expressing high levels of dysfunctional PPARγ, which suppressed normal-function PPARγ. The mice developed high blood pressure levels and severe vascular dysfunction resembling the hallmarks of advanced diabetes.
正如研究者们发表在《细胞代谢》杂志上的那样，失去功能的（PPAR）γ在这些小鼠上表达水平高，而功能正常的（PPAR）γ表达则减少。这些小鼠有更高的血压水平，并存在严重的血管功能的丧失，这些都是糖尿病进展的标志。
Aortic tissue taken from these mice showed reduced contractility in response to vasodilating nitric oxide and hypercontractility in response to the potent vasoconstrictor endothelin-1.
从这些小鼠上获得的大动脉组织对扩血管药物一氧化氮的反应性减少，对血管所收缩剂内皮素的反应过度。
Further analysis showed that cerebral arterioles of mice expressing dysfunctional PPARγ underwent hypertrophy, with an increase in distensibility and remodeling and reduction in external diameter.
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作者:admin@医学,生命科学 2011-04-02 05:14
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