Effects of chronic exercise on calcium signaling in rat vascular endothelium

Chu, Tzu-Fang; Huang, Tzu-Yuan; Jen, Chauying J.; Chen, Hsiun‐ing

doi:10.1152/ajpheart.2000.279.4.h1441

Cited by 17 publications

(18 citation statements)

References 29 publications

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“…Furthermore, Steinert et al (2002) and Mahdy et al (1998) demonstrated that human fetal venous EC and maternal human hand vein EC show a loss of the sustained phase in subjects with preeclampsia, a condition that is characterized by hypertension (Mahdy et al 1998, Steinert et al 2002. This data along with our previous data on UAEC led us to believe that the sustained phase of the [Ca 2C ] i response in NP-UAEC is relatively unresponsive, while P-UAEC mobilize Ca 2C more like calf pulmonary artery EC, bovine aortic EC, and rat aortic EC (Chu et al 2000, Bishara et al 2002, Wilkinson & Jacob 2003.…”

Section: Introductionsupporting

confidence: 58%

Pregnancy-enhanced store-operated Ca2+ channel function in uterine artery endothelial cells is associated with enhanced agonist-specific transient receptor potential channel 3-inositol 1,4,5-trisphosphate receptor 2 interaction

Gifford¹,

Feng²,

Bird³

2006

Journal of Endocrinology

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We have previously shown that endothelial cells (EC) derived from the uterine artery (UA) of both pregnant (P-UAEC) and nonpregnant (NP-UAEC) ewes show a biphasic intracellular free Ca 2C ([Ca 2C ] i ) response after ATP stimulation. In each case, the initial transient peak, caused by the release of Ca 2C from the intracellular Ca 2C stores, is mediated by purinergic receptor-Y2 and is very similar in both cell types. However, the sustained phase in particular, caused by the influx of extracellular Ca 2C, is heightened in the P-UAEC, and associates with an increased ability of the cells to demonstrate enhanced capacitative Ca 2C entry (CCE) via store-operated channels (SOCs). Herein we demonstrated that the difference in the sustained [Ca 2C ] i response is maintained for at least 30 min. When 2-aminoethoxydiphenyl borate (2APB) (an inhibitor of the inosital 1,4,5-trisphosphate receptor (IP3R) and possibly SOC) was used in conjunction with ATP, it was capable of completely inhibiting CCE. Since 2APB can inhibit SOC in some cell types and 2APB was capable of inhibiting CCE in the UAEC model, the role of SOC in CCE was first evaluated using the classical inhibitor La ] i response. Since canonical transient receptor potential channels (TRPCs) have recently been identified as putative SOCs in many cell types, including EC, the expression levels of several isoforms were evaluated in UAEC. Expression of TRPC3 and TRPC6 channels in particular was detected, but no significant difference in expression level was found between NP-and P-UAEC. Nonetheless, we were able to show that IP3R2 interacts with TRPC3 in UAEC, forming a protein complex, and that this interaction is considerably enhanced in an agonist sensitive manner by pregnancy. Thus, while IP3R and TRPC isoforms are not altered in their expression by pregnancy, enhanced functional interaction of TRPC3 with IP3R2 may underlie pregnancy-enhanced CCE in the UAEC model and so explain the prolonged [Ca 2C ] i sustained phase seen in response to ATP.

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Section: Introductionsupporting

confidence: 58%

Pregnancy-enhanced store-operated Ca2+ channel function in uterine artery endothelial cells is associated with enhanced agonist-specific transient receptor potential channel 3-inositol 1,4,5-trisphosphate receptor 2 interaction

Gifford¹,

Feng²,

Bird³

2006

Journal of Endocrinology

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“…Thus, although acute exercise increased the vascular responses to endothelium-dependent vasodilators (such as ACh), data points from the exercise group only extended to high levels of EC [Ca 2ϩ ] i elevations that accompanied a little additional vasorelaxation. In separate studies, we found that chronic exercise enhances ACh-induced vasorelaxation (4,6) and the EC [Ca 2ϩ ] i response (9). Perhaps the chronic exercise also affects vasorelaxation by altering EC [Ca 2ϩ ] i signaling.…”

Section: Comparison Of Ach-induced Calcium Responses and Vasorelaxatimentioning

confidence: 90%

“…The basic setup for EC [Ca 2ϩ ]i imaging was similar to that described in our previous reports (9,13). Fura 2-loaded vessel rings were opened longitudinally and pinned to the base plate of a tissue flow chamber.…”

Section: Methodsmentioning

confidence: 99%

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Acute exercise enhances vasorelaxation by modulating endothelial calcium signaling in rat aortas

Jen

Chan

Chen

2002

American Journal of Physiology-Heart and Circulatory Physiology

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The role of endothelial calcium signaling in exercise-enhanced ACh-induced vasorelaxation was examined using male Wistar rats (8∼10 wk old) that were divided into control and exercise groups. The exercised animals ran on a treadmill with progressive increments of speed until exhaustion. After decapitation, aortic rings were dissected and loaded with fura 2-AM. After being mounted on a tissue flow chamber, vessels were precontracted with phenylephrine, and ACh-induced endothelial calcium elevation and vasorelaxation were determined simultaneously under an epifluorescence microscope equipped with ratio imaging capability. Our results showed that 1) there was logarithmic correlation between endothelial calcium elevation and vasorelaxation; 2) acute exercise enhanced ACh-induced endothelial calcium elevation and vasorelaxation without altering their relationship; 3) pretreatment with N ω-nitro-l-arginine markedly reduced ACh-induced vasorelaxation in both groups but suppressed the calcium response only in the exercise group; and 4) the exercise effect on endothelial calcium elevation was abolished by Ca2+-free buffer or gadolinium. In conclusion, acute exercise increases ACh-induced vasorelaxation by increasing the endothelial calcium influx and the calcium-dependent nitric oxide release.

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“…Therefore, the exercise-induced changes are likely due to local increases in blood flow or shear stress instead of to systemic changes in the plasma hormone levels. Our laboratory's previous studies with rat aortic specimens (7,17) have shown that chronic exercise or flow pretreatment of vascular segments increases ACh-induced intracellular calcium elevation in endothelium, which is one of the major upstream signals in endothelium-derived NO production. As the promoter region of eNOS gene contains a shear stress-responsive element (20), exercise training may upregulate eNOS gene expression by an increase in shear stress, and then facilitate NO release.…”

Section: Discussionmentioning

confidence: 99%

Effects of high-cholesterol diet and parallel exercise training on the vascular function of rabbit aortas: a time course study

Yang

Jen

Chen

2003

Journal of Applied Physiology

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Effects of high-cholesterol diet and parallel exercise training on the vascular function of rabbit aortas: a time course study. J Appl Physiol 95: 1194-1200, 2003. First published May 16, 2003 10.1152/japplphysiol.00282.2003It is plausible to assume that exercise training, when applied early enough, can completely correct atherosclerotic defects. Using rabbit aortic specimens, we examined the effects of chronic exercise and high-cholesterol diet feeding on vascular function for different time periods. Male New Zealand White rabbits were divided into four groups: the normal diet groups with or without exercise training and the high-cholesterol diet groups with or without exercise training. Animals in highcholesterol diet groups were fed 2% cholesterol rabbit chow for 2, 4, or 6 wk. Those in exercise training groups ran on a treadmill at 0.88 km/h for up to 40 min/day, 5 days/wk for the same period of time as the diet feeding. Thoracic aortas were isolated for functional and immunohistochemical analyses. We found that 1) although high-cholesterol diet feeding (Ն2 wk) elevated serum cholesterol levels and impaired acetylcholine-evoked vasorelaxation, only the latter effect was reversed by exercise training; 2) the effects of diet and exercise on acetylcholine-evoked vasorelaxation were mainly due to altered release of nitric oxide and endothelium-derived hyperpolarizing factor; and 3) diet feeding for 4 or 6 wk caused significant lipid deposition and expression of P-selectin, VCAM-1, monocyte chemoattractant protein-1, and inducible nitric oxide synthase, which were largely reduced by exercise training. In conclusion, parallel exercise training almost completely reverses the early-stage endothelial dysfunction caused by high-cholesterol diet feeding. endothelium; acetylcholine; adhesion molecules; inflammation; nitric oxide synthase ATHEROGENESIS IS ASSOCIATED WITH vascular dysfunction, which is possibly caused by hypercholesterolemia, hypertension, smoking, diabetes mellitus, and genetic alterations. Moreover, endothelial dysfunction has been proposed to be the initial event during the progression of atherosclerosis (19,25). Normally, the vascular endothelium releases various vasorelaxing factors, notably nitric oxide (NO) (24), which not only relaxes the vascular smooth muscle but also inhibits low-density lipoprotein (LDL) oxidation, platelet/ monocyte adhesion, and smooth muscle proliferation/ migration. Therefore, NO is widely accepted as an endogenous antiatherosclerotic factor (3). Previous studies have demonstrated that endothelial NO synthase (eNOS) expression and NO release are markedly reduced, whereas the expression of inducible NO synthase (iNOS) is increased in the vessels of high cholesterol-fed animals or in human atherosclerotic lesions (2,4,22). In addition, the expression of vascular adhesion molecules, such as P-selectin and vascular cell adhesion molecule 1 (VCAM-1), is elevated in the early stage of atherogenesis (9, 15). Finally, monocyte chemoattractant protein-1 (MCP-1) in atherosclerotic ...

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Effects of chronic exercise on calcium signaling in rat vascular endothelium

Cited by 17 publications

References 29 publications

Pregnancy-enhanced store-operated Ca2+ channel function in uterine artery endothelial cells is associated with enhanced agonist-specific transient receptor potential channel 3-inositol 1,4,5-trisphosphate receptor 2 interaction

Pregnancy-enhanced store-operated Ca2+ channel function in uterine artery endothelial cells is associated with enhanced agonist-specific transient receptor potential channel 3-inositol 1,4,5-trisphosphate receptor 2 interaction

Acute exercise enhances vasorelaxation by modulating endothelial calcium signaling in rat aortas

Effects of high-cholesterol diet and parallel exercise training on the vascular function of rabbit aortas: a time course study

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