Transient receptor potential channels in essential hypertension

Liu, Daoyan; Scholze, Alexandra; Zhu, Zhiming; Krueger, Katharina; Thilo, Florian; Burkert, Antje; Streffer, Katrin; Holz, S; Harteneck, Christian; Zidek, Walter; Tepel, Martín

doi:10.1097/01.hjh.0000226201.73065.14

Cited by 65 publications

(54 citation statements)

References 49 publications

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“…The specific targeted sequence of TRPC5 was sense, 5Ј-GGAGGCUGAGAUCUACUAUtt-3Ј; and antisense, 5Ј-AUAGUAGAUCUCAGCCUCCtg-3Ј (Liu et al, 2006). ECs at 80% confluence were incubated with siRNA duplex of TRPC5 (20 nM final concentration) for 24 h using the transfection kit (RNAiFect, Qiagen) and following the manufacturer's protocol.…”

Section: Down-regulation Of Trpc Mrnamentioning

confidence: 99%

Elucidation of a TRPC6-TRPC5 Channel Cascade That Restricts Endothelial Cell Movement

Chaudhuri

Colles²,

Wagoner³

et al. 2008

MBoC

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Section: Down-regulation Of Trpc Mrnamentioning

confidence: 99%

Elucidation of a TRPC6-TRPC5 Channel Cascade That Restricts Endothelial Cell Movement

Chaudhuri

Colles²,

Wagoner³

et al. 2008

MBoC

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“…Dietrich et al 4 reported that TRPC6-deficient mice with consecutively increased TRPC3 channel expression developed higher blood pressure. Liu et al 5,6 and Thilo et al 7 reported increased TRPC3 protein expression and increased TRPC3 transcripts in peripheral blood monocytes from patients with essential hypertension compared to normotensive control subjects. The expression of TRPC3 in human vascular endothelium has not been associated with malignant hypertension yet.…”

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confidence: 99%

Increased TRPC3 expression in vascular endothelium of patients with malignant hypertension

et al. 2009

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An increased expression of transient receptor potential canonical type 3 (TRPC3) cation channels has been proposed as one of the factors contributing to the pathogenesis of hypertension. To test that hypothesis we compared the expression of TRPC3 and TRPC6 as an endogenous control in human vascular endothelium of preglomerular arterioles in kidney biopsies from six patients with malignant hypertension and from four patients with diarrhea-associated hemolytic-uremic syndrome. Patients with malignant hypertension showed significantly higher systolic blood pressure and more prominent expression of TRPC3 in vascular endothelium of preglomerular arterioles compared to patients with hemolytic-uremic syndrome. The expression of TRPC6 was not different between the two groups. The study supports the hypothesis that the increased expression of TRPC3 is associated with malignant hypertension in humans. Malignant hypertension is a hypertensive emergency with severe elevation of blood pressure, a Keith-Wagener-Barker grade III or IV hypertensive retinopathy, and acute impairment of renal function in most cases. In white subjects, essential hypertension accounts for approximately 30% of malignant hypertension, whereas in blacks essential hypertension is the predominant cause, accounting for approximately 82% of all cases. The characteristic pathological change of malignant hypertension represents endothelial injury. Its pathophysiology involves mechanical stress on the vessel wall, a proliferative endarteriitis in small arteries and arterioles, and fibrinoid necrosis with fine subendothelial droplets and hyalin thrombi formation.

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“…In addition, increased TRPC3 and TRPC5 expression in monocytes of patients with essential hypertension, a subsequent storeoperated Ca 2+ influx, and increased 1-oleoyl-2-acetyl-snglycerol-induced cation influx in monocytes of patients with essential hypertension were observed [61]. Liu et al [1] compared the expression level and function of TRPCs between essential hypertensive patients and normotensive control subjects. They demonstrated increased TRPC3 and TRPC5 protein expression and an increase in the gadolinium/calcium-influx ratio via TRPCs in monocytes of patients with essential hypertension [1].…”

Section: Trp Channel Subtype C Dysfunction Promotes the Development Omentioning

confidence: 99%

“…Liu et al [1] compared the expression level and function of TRPCs between essential hypertensive patients and normotensive control subjects. They demonstrated increased TRPC3 and TRPC5 protein expression and an increase in the gadolinium/calcium-influx ratio via TRPCs in monocytes of patients with essential hypertension [1]. Furthermore, they demonstrated an increase in TRPC3 expression in VSMCs and aortic tissues and TRPC3-related Ca 2+ influx in VSMCs from spontaneously hypertensive rats (SHRs), which was associated with enhanced contraction in vasculature from SHRs compared with the normotensive WKY rats [4].…”

Section: Trp Channel Subtype C Dysfunction Promotes the Development Omentioning

confidence: 99%

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Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension

Liu

Xiong

Zhu

2014

Sci. China Life Sci.

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Intracellular Ca 2+ homeostasis is essential for vascular function and blood pressure regulation. Because of their unique roles in regulating intracellular Ca 2+ concentration and vascular function, a novel class of non-selective cation channels, called transient receptor potential (TRP) channels, have emerged at the frontier of hypertension research. Based on their role in vasculature function regulation, TRP channels can be divided into two functional subtypes: one that participates in vasoconstriction and one that participates in vasodilatation. A functional imbalance of these two subtypes of TRP channels may disturb intracellular calcium ([Ca 2+ ]i) homeostasis, and the consequent vascular dysfunction may contribute to the development of hypertension. The potential of these TRP channels as novel pharmacological targets for the treatment of human hypertension is of great interest. TRP channels, Ca 2+ homeostasis, vascular function, hypertension Citation:Liu DY, Xiong SQ, Zhu ZM. Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension. Sci China Life Sci, 2014, 57: 818 -825,

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Transient receptor potential channels in essential hypertension

Abstract: This study points to an important role of TRPCs in essential hypertension.

Cited by 65 publications

References 49 publications

Elucidation of a TRPC6-TRPC5 Channel Cascade That Restricts Endothelial Cell Movement

Elucidation of a TRPC6-TRPC5 Channel Cascade That Restricts Endothelial Cell Movement

Increased TRPC3 expression in vascular endothelium of patients with malignant hypertension

Imbalance and dysfunction of transient receptor potential channels contribute to the pathogenesis of hypertension

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