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Mechanisms involved in the relaxation of bovine aortic endothelial cells.

机译：牛主动脉内皮细胞松弛涉及的机制。

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The importance of endothelial cell contraction in the regulation of vascular biology is being increasingly recognized. Our group has demonstrated that reactive oxygen species, particularly hydrogen peroxide, which are released in pathological conditions such as ischemia-reperfusion, are able to induce contraction in bovine aortic endothelial cells (BAEC). The cGMP-dependent relaxation of contractile cells depends on the ability of the cyclic nucleotide to interfere with intracellular calcium; however, this is not the only mechanism involved. The present experiments were designed to analyse the mechanism by which cGMP induces relaxation in BAEC. Sodium nitroprusside (SNP), an activator of soluble guanylate cyclase, as well as atrial natriuretic (ANP) and C-type natriuretic (CNP) peptides, activators of particulate guanylate cyclase, blunted the hydrogen peroxide-induced contraction of BAEC and myosin light chain phosphorylation. The inhibitory effect was more marked with SNP and CNP than with ANP, and the action of SNP and CNP were partially reversed by blocking soluble and particulate guanylate cyclases, respectively. Dibutyryl cGMP (db-cGMP), a cGMP analogue, mimicked the effect of SNP and CNP. Cyclic GMP-dependent protein kinase (cGK) protein levels and activity were measured. Hydrogen peroxide induced a significant reduction in cGK activity without any change in protein level. This effect was completely reversed by preincubation with db-cGMP. Calyculin A, a myosin light chain phosphatase inhibitor, prevented the cGMP-induced relaxation of BAEC. SNP, CNP and db-cGMP also partially prevented the hydrogen peroxide-induced increase in intracellular calcium levels. Catalase completely blocked this effect. In summary, the present results support a role for those metabolites which activate guanylate cyclases in the relaxation of BAEC, and suggest that the cGMP-induced BAEC relaxation could be due, at least partially, to the stimulation of cGK and/or myosin light chain phosphatase activity, and to calcium blockade.
机译：内皮细胞收缩在调节血管生物学中的重要性日益得到认可。我们的研究小组证明，在缺血性再灌注等病理条件下释放的活性氧，特别是过氧化氢，能够诱导牛主动脉内皮细胞（BAEC）收缩。收缩细胞依赖cGMP的松弛取决于环状核苷酸干扰细胞内钙的能力。但是，这不是唯一的机制。本实验旨在分析cGMP诱导BAEC松弛的机制。可溶性鸟苷酸环化酶的激活剂硝普钠（SNP），以及鸟苷酸环化酶的激活剂心房利钠（ANP）和C型利尿钠（CNP）肽抑制了过氧化氢诱导的BAEC和肌球蛋白轻链的收缩磷酸化。 SNP和CNP的抑制作用比ANP更为明显，并且分别阻断可溶性鸟苷酸环化酶和颗粒鸟苷酸环化酶可部分逆转SNP和CNP的作用。 cGMP类似物二丁酰cGMP（db-cGMP）模仿了SNP和CNP的作用。测量了环状GMP依赖性蛋白激酶（cGK）的蛋白水平和活性。过氧化氢诱导cGK活性显着降低，而蛋白质水平没有任何变化。通过与db-cGMP一起预孵育可以完全逆转这种效果。 Calyculin A是一种肌球蛋白轻链磷酸酶抑制剂，可防止cGMP诱导的BAEC松弛。 SNP，CNP和db-cGMP还可部分阻止过氧化氢诱导的细胞内钙水平升高。过氧化氢酶完全阻断了这种作用。总之，本研究结果支持了激活鸟苷酸环化酶的那些代谢物在BAEC松弛中的作用，并暗示cGMP诱导的BAEC松弛可能至少部分地是由于cGK和/或肌球蛋白轻链的刺激所致。磷酸酶的活性，并能阻断钙。

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