What question did this study set out to answer?

To investigate whether store depletion-induced endothelium-dependent vascular relaxations and store-operated calcium entry are impaired in aging rat thoracic aorta.

June 1, 2016Acta Physiologica HungaricaOpen Access

Alterations of store-operated calcium entry and cyclopiazonic acid-induced endothelium-derived relaxations in aging rat thoracic aorta

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Authors

YEYasemin EraçEge University ÇSÇiğdem SelliBoston University MTMetiner TosunIzmir University

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Implication

Ex vivo animal study shows reduced store-operated calcium entry and TRPC4 expression in aging rat aorta, indicating mechanisms behind age-related endothelial dysfunction.

Key Points

To investigate whether store depletion-induced endothelium-dependent vascular relaxations and store-operated calcium entry are impaired in aging rat thoracic aorta.
Vascular responses to acetylcholine (ACh), cyclopiazonic acid (CPA), and sodium nitroprusside were evaluated in aortic rings from young (2–4 month) and old (20–24 month) male Sprague-Dawley rats.
Intracellular calcium shifts following CPA stimulation were measured via fura-2 fluorescence in endothelium-denuded aortic segments.
TRPC4 expression was quantified using real-time quantitative RT-PCR and Western blot analysis in aortic tissues.
Both ACh- and CPA-induced endothelium-dependent relaxations significantly decreased in old rat aorta compared to young controls, whereas direct vasodilation by sodium nitroprusside remained unaffected.
CPA-induced store-operated calcium entry (SOCE) significantly declined in endothelium-denuded aging aorta, while sarcoplasmic reticulum calcium release remained unchanged.
Endothelial TRPC4 mRNA and total intact aortic TRPC4 protein levels decreased significantly in 20- to 24-month-old rats compared to 2- to 4-month-old rats.

Cite This Study

Eraç et al. (2016) studied this question.

synapsesocial.com/papers/6a73798fe7786f1b8071ae3e https://doi.org/10.1556/036.103.2016.2.2

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Implication

Ex vivo animal study shows reduced store-operated calcium entry and TRPC4 expression in aging rat aorta, indicating mechanisms behind age-related endothelial dysfunction.

Alterations of store-operated calcium entry and cyclopiazonic acid-induced endothelium-derived relaxations in aging rat thoracic aorta

Discussion

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Implication

Key Points

Cite This Study

Alterations of store-operated calcium entry and cyclopiazonic acid-induced endothelium-derived relaxations in aging rat thoracic aorta

Discussion

Member takes

Implication

Key Points

Cite This Study

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