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用Fura-2作为探针来显示,在喂食高盐饮食的Dahl敏感型大鼠的血小板中,细胞内游离钙升高。

Fura-2 used as a probe to show elevated intracellular free calcium in platelets of Dahl-sensitive rats fed a high salt diet.

作者信息

Vasdev S, Thompson P, Triggle C, Fernandez P, Bolli P, Ananthanarayanan V S

机构信息

Disciplines of Medicine, Memorial University, St. John's, Newfoundland, Canada.

出版信息

Biochem Biophys Res Commun. 1988 Jul 15;154(1):380-6. doi: 10.1016/0006-291x(88)90696-1.

Abstract

Elevated intracellular free calcium concentration [Ca2+]i in vascular smooth muscle cells has been implicated in the pathophysiology of hypertension. Platelet [Ca2+]i was measured using the fluorescent indicator, Fura-2, in Dahl sensitive (DS) and resistant (DR) rats given high (8% NaCl) and low (0.4% NaCl) salt diets, as well as in the spontaneously hypertensive (SHR) and Wistar-Kyoto (WKY) rats. The aim of this study was to show whether [Ca2+]i is elevated in salt induced hypertension. Platelet [Ca2+]i and systolic blood pressure (SBP) were higher (p less than 0.001) in DS rats given a high than low salt diets. In contrast, no changes in platelet [Ca2+]i and SBP were observed in DR rats. In SHR, platelet [Ca2+]i and SBP were higher (p less than 0.001) than in the WKY rats. Platelet [Ca2+]i correlated with SBP in all groups of rats (r = 0.929; p less than 0.001, n = 38). The parallel increase in SBP and [Ca2+]i in the DS high salt rats and the SHR suggests that an increased [Ca2+]i is involved in the pathophysiology of hypertension in the two models which differ with respect to the pathogenesis of their hypertension. This increase in [Ca2+]i therefore seems to reflect an abnormality in [Ca2+]i handling in hypertension regardless of its cause.

摘要

血管平滑肌细胞内游离钙浓度[Ca2+]i升高与高血压的病理生理学有关。使用荧光指示剂Fura-2测量给予高盐(8%氯化钠)和低盐(0.4%氯化钠)饮食的Dahl敏感(DS)和抗性(DR)大鼠以及自发性高血压(SHR)和Wistar-Kyoto(WKY)大鼠的血小板[Ca2+]i。本研究的目的是表明在盐诱导的高血压中[Ca2+]i是否升高。给予高盐饮食的DS大鼠的血小板[Ca2+]i和收缩压(SBP)高于给予低盐饮食的大鼠(p<0.001)。相比之下,DR大鼠的血小板[Ca2+]i和SBP没有变化。在SHR中,血小板[Ca2+]i和SBP高于WKY大鼠(p<0.001)。所有组大鼠的血小板[Ca2+]i与SBP相关(r = 0.929;p<0.001,n = 38)。DS高盐大鼠和SHR中SBP和[Ca2+]i的平行升高表明,[Ca2+]i升高参与了这两种高血压发病机制不同的模型的高血压病理生理学。因此,这种[Ca2+]i的升高似乎反映了高血压中[Ca2+]i处理的异常,无论其原因如何。

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