Elsevier

Life Sciences

Volume 54, Issue 9, 1994, Pages PL153-PL158
Life Sciences

Pharmacology letter
Thapsigargin, A Ca2+-ATPase inhibitor, relaxes rat aorta via nitric oxide formation

https://doi.org/10.1016/0024-3205(94)00875-2Get rights and content

Abstract

Thapsigargin induced endothelium-dependent relaxation and cGMP production in rat thoracic aorta, and these effects were inhibited by nitric oxide (NO) pathway inhibitors, a calmodulin inhibitor and removal of Ca2+, suggesting that NO is involved in the thapsigargin-induced relaxation. Thapsigargin may deplete Ca2+ stores in the endothelial cells by inhibiting the CA2+-ATPase, a Ca2+ pump, which in turn triggers influx of extracellular Ca2+, leading to activation of constitutive NO synthase and resultant NO generation. The NO thus formed may activate soluble guanylate cyclase to produce cGMP in the vascular smooth muscle.

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