Impaired capsaicin-induced relaxation in diabetic mesenteric arteries

Zhang, Yuanyuan; Chen, Qiang; Sun, Zewei; Han, Jie; Wang, Lihong; Zheng, Liangrong

doi:10.1016/j.jdiacomp.2015.05.005

Cited by 13 publications

(15 citation statements)

References 26 publications

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“…Noteworthy, the protective effects persisted when NOD pre-treatment was suspended and only post-IRI treatment was carried out. Furthermore, NOD failed to protect renal allograft recipients from AKI which contrasts the work of Spindler et al Interestingly, the observed improvement in renal function by NOD was not associated with putatively TRPV1 induced large increases in kidney perfusion as measured by magnetic resonance imaging (Klotz et al 2016), which is unexpected as TRPV1 activation is a potent mechanism to produce vasodilation in the renal circulation (Chen et al 2015).…”

Section: Trpv1mentioning

confidence: 67%

“…The vasodilatory effects are NOdependent but independent from TRPV1 activation in these vessels ( Fig. 1) (Chen et al 2015). The role of NO as a downstream effector of TRPV4-dependent relaxation is not an universal finding for all vessels as NO-independent vasodilation in response to TRPV4 activation was observed in other vascular preparations (Marrelli et al 2007, Sonkusare et al 2012, Cabral & Garvin 2014.…”

Section: Trpv4mentioning

confidence: 85%

“…Of note, the observed impairment was found to be dependent of endothelial nitric oxide (NO) (Zhang et al . ). TRPV1 expression and signalling is also reduced in diabetic hearts (Zheng et al .…”

Section: Transient Receptor Potential Channelsmentioning

confidence: 97%

“…1). Importantly, Ca 2+ influx through TRPV1 channels causes relaxation of renal resistance arteries, but not renal conduit arteries or vasa recta (Chen et al 2015). Thus, TRPV1 lacks functional expression in descending vasa recta (DVR) (Fig.…”

Section: Trpv1mentioning

confidence: 99%

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Renoprotection: focus on TRPV1, TRPV4, TRPC6 and TRPM2

et al. 2016

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Members of the transient receptor potential (TRP) cation channel receptor family have unique sites of regulatory function in the kidney which enables them to promote regional vasodilatation and controlled Ca influx into podocytes and tubular cells. Activated TRP vanilloid 1 receptor channels (TRPV1) have been found to elicit renoprotection in rodent models of acute kidney injury following ischaemia/reperfusion. Transient receptor potential cation channel, subfamily C, member 6 (TRPC6) in podocytes is involved in chronic proteinuric kidney disease, particularly in focal segmental glomerulosclerosis (FSGS). TRP vanilloid 4 receptor channels (TRPV4) are highly expressed in the kidney, where they induce Ca influx into endothelial and tubular cells. TRP melastatin (TRPM2) non-selective cation channels are expressed in the cytoplasm and intracellular organelles, where their inhibition ameliorates ischaemic renal pathology. Although some of their basic properties have been recently identified, the renovascular role of TRPV1, TRPV4, TRPC6 and TRPM2 channels in disease states such as obesity, hypertension and diabetes is largely unknown. In this review, we discuss recent evidence for TRPV1, TRPV4, TRPC6 and TRPM2 serving as potential targets for acute and chronic renoprotection in chronic vascular and metabolic disease.

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Section: Trpv1mentioning

confidence: 67%

Section: Trpv4mentioning

confidence: 85%

Section: Transient Receptor Potential Channelsmentioning

confidence: 97%

Section: Trpv1mentioning

confidence: 99%

See 2 more Smart Citations

Renoprotection: focus on TRPV1, TRPV4, TRPC6 and TRPM2

et al. 2016

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“…In these tissues, activation of TRPV1 by capsaicin resulted in endothelium-independent vasoconstriction, decreased hind limb perfusion, and increased gracilis muscle vascular resistance (733, 1034, 1467). TRPV1 activation can also cause vasodilation, but this is in an endothelium-dependent manner and not attributed to SMC TRPV1 (1626). …”

Section: Transient Receptor Potential Channelsmentioning

confidence: 99%

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

Tykocki

Boerman

Jackson

2017

Comprehensive Physiology

272

347

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Vascular tone of resistance arteries and arterioles determines peripheral vascular resistance, contributing to the regulation of blood pressure and blood flow to, and within the body’s tissues and organs. Ion channels in the plasma membrane and endoplasmic reticulum of vascular smooth muscle cells (SMCs) in these blood vessels importantly contribute to the regulation of intracellular Ca2+ concentration, the primary determinant of SMC contractile activity and vascular tone. Ion channels provide the main source of activator Ca2+ that determines vascular tone, and strongly contribute to setting and regulating membrane potential, which, in turn, regulates the open-state-probability of voltage gated Ca2+ channels (VGCCs), the primary source of Ca2+ in resistance artery and arteriolar SMCs. Ion channel function is also modulated by vasoconstrictors and vasodilators, contributing to all aspects of the regulation of vascular tone. This review will focus on the physiology of VGCCs, voltage-gated K+ (KV) channels, large-conductance Ca2+-activated K+ (BKCa) channels, strong-inward-rectifier K+ (KIR) channels, ATP-sensitive K+ (KATP) channels, ryanodine receptors (RyRs), inositol 1,4,5-trisphosphate receptors (IP3Rs), and a variety of transient receptor potential (TRP) channels that contribute to pressure-induced myogenic tone in resistance arteries and arterioles, the modulation of the function of these ion channels by vasoconstrictors and vasodilators, their role in the functional regulation of tissue blood flow and their dysfunction in diseases such as hypertension, obesity, and diabetes.

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Mechanism of capsaicin inhibition of aldose reductase activity

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Kılınç

Şengül

et al. 2017

J Biochem & Molecular Tox

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Aldose reductase (AR) inhibitors play a vital importance as a potential therapeutic and preventive medicine when it comes to hyperglycemia associated diabetic complications. Additionally, capsaicin is used as a food additive and a drug in a number of diverse clinical trials. The aim of this study is to determine the in vitro inhibition behavior of capsaicin on AR enzyme activity, which was obtained from different rat tissues (heart, kidney, liver, and brain). We showed that AR was inhibited by capsaicin in the micromolar range and noncompetitive manner in all of the tissues. K values of capsaicin were found to be 8.87, 264, 535, and 597, respectively, in heart AR, kidney AR, liver AR, and brain AR. In conclusion, capsaicin may be an effective molecule when used in low concentrations to prevent diabetic complications associated with the polyol pathway.

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Impaired capsaicin-induced relaxation in diabetic mesenteric arteries

Cited by 13 publications

References 26 publications

Renoprotection: focus on TRPV1, TRPV4, TRPC6 and TRPM2

Renoprotection: focus on TRPV1, TRPV4, TRPC6 and TRPM2

Smooth Muscle Ion Channels and Regulation of Vascular Tone in Resistance Arteries and Arterioles

Mechanism of capsaicin inhibition of aldose reductase activity

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