Deletion of T-type calcium channels Cav 3.1 or Cav 3.2 attenuates endothelial dysfunction in aging mice

Pflügers Archiv : European journal of physiology
Anne D ThuesenPernille B L Hansen

Abstract

Impairment of endothelial function with aging is accompanied by reduced nitric oxide (NO) production. T-type Cav3.1 channels augment nitric oxide and co-localize with eNOS. Therefore, the hypothesis was that T-type channels contribute to the endothelial dysfunction of aging. Endothelial function was determined in mesenteric arteries (perfusion) and aortae (isometric contraction) of young and old wild-type (WT), Cav3.1, and Cav3.2 knockout mice. NO production was measured by fluorescence imaging in mesenteric arteries. With age, endothelium-dependent subsequent dilatation (following depolarization with KCl) of mesenteric arteries was diminished in the arteries of WT mice, unchanged in Cav3.2-/- preparations but increased in those of Cav3.1-/- mice. NO synthase inhibition abolished the subsequent dilatation in mesenteric arteries and acetylcholine-induced relaxations in aortae. NO levels were significantly reduced in mesenteric arteries of old compared to young WT mice. In Cav3.1-/- and Cav3.2-/- preparations, NO levels increased significantly with age. Relaxations to acetylcholine were significantly smaller in the aortae of old compared to young WT mice, while such responses were comparable in preparations of young and old Cav3....Continue Reading

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Citations

Jun 21, 2019·Journal of Medical Genetics·Norbert Weiss, Gerald W Zamponi
Oct 28, 2021·The Journal of Physiology·Osama F Harraz, Lars Jørn Jensen

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Methods Mentioned

BETA
force measurements
protein assay

Software Mentioned

gskb R - package
Lab View
Affymetrix® Expression [UNK]
PGSEA R - package

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