Vollrath B, Weir B K, Cook D A
Department of Pharmacology, University of Alberta, Edmonton, Canada.
Biochem Biophys Res Commun. 1990 Aug 31;171(1):506-11. doi: 10.1016/0006-291x(90)91422-o.
To test the hypothesis that oxyhemoglobin causes contraction of vascular smooth muscle by production of inositol 1,4,5-trisphosphate which results in a release of intracellular calcium, smooth muscle cells were exposed to oxyhemoglobin and inositol trisphosphate was measured. Oxyhemoglobin, but not methemoglobin which has much less contractile action, stimulated inositol trisphosphate production. The time course was consistent with an early role for this compound in the contraction produced by hemoglobin. The increase in production of inositol trisphosphate was inhibited by pertussis toxin and also by neomycin, an inhibitor of phospholipase C, although the actions of the latter compound cannot be attributed only to an inhibition of the enzyme responsible for the production of inositol trisphosphate.
为了验证氧合血红蛋白通过产生肌醇1,4,5 -三磷酸导致细胞内钙释放从而引起血管平滑肌收缩这一假说，将平滑肌细胞暴露于氧合血红蛋白中并检测肌醇三磷酸。氧合血红蛋白能刺激肌醇三磷酸的产生，而具有较弱收缩作用的高铁血红蛋白则不能。其时间进程与该化合物在血红蛋白引起的收缩中起早期作用一致。百日咳毒素和磷脂酶C抑制剂新霉素均可抑制肌醇三磷酸生成的增加，尽管后一种化合物的作用不能仅归因于对负责肌醇三磷酸生成的酶的抑制。
